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The Interleukin-1 Family: Back to the Future
Open accessAbstract
Interleukin-1 (IL-1) is a central mediator of innate immunity and inflammation. The IL-1 family includes seven ligands with agonist activity (IL-1α and IL-1β, IL-18, IL-33, IL-36α, IL-36β, IL-36γ), three receptor antagonists (IL-1Ra, IL-36Ra, IL-38), and an anti-inflammatory cytokine (IL-37). Members of the IL-1 Receptor (IL-1R) family include six receptor chains forming four signaling receptor complexes, two decoy receptors (IL-1R2, IL-18BP), and two negative regulators (TIR8 or SIGIRR, IL-1RAcPb). A tight regulation via receptor antagonists, decoy receptors, and signaling inhibitors ensures a balance between amplification of innate immunity and uncontrolled inflammation. All cells of the innate immune system express and/or are affected by IL-1 family members. Moreover, IL-1 family members play a key role in the differentiation and function of polarized innate and adaptive lymphoid cells. Here we will review the key properties of IL-1 family members, with emphasis on pathways of negative regulation and orchestration of innate and adaptive immunity.
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“In addition, NLRP3 inflammasome activation reduces phagocytosis of Aβ by microglial cells, thus increasing the Aβ depositions and contributing to the pathogenesis of AD (Garlanda et al., 2013; Gold and El Khoury, 2015).”
From The role of microglia in retinal neurodegeneration: Alzheimer’s disease, parkinson, and glaucoma. (2017) · cites this paper as Garlanda et al., 2013
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“Interleukin-18 is a member of the large interleukin-1 family40 that has recently been associated with cytokine storm disorders.”
From Cytokine storm (2020) · cites this paper as [40]
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Mantovani, A., Allavena, P., Sica, A., & Balkwill, F. (2008) · Nature · doi:10.1038/nature07205 · Cited by 11,399
Self-citationSuccinate is an inflammatory signal that induces IL-1β through HIF-1α
Tannahill, G. M., Curtis, A. M., Adamik, J., Palsson-McDermott, E. M., McGettrick, A. F., Goel, G., Frezza, C., Bernard, N. J., Kelly, B., Foley, N. H., et al. (2013) · Nature · doi:10.1038/nature11986 · Cited by 4,176 · cited 1×
“Accumulation of succinate in classically Immunity 39, December 12, 2013 ª2013 Elsevier Inc. 1005 activatedM1macrophages (Tannahill et al., 2013) stabilizes hypoxia-inducible factor a (HIF-1a), which in turn induces IL-1b.”
Veldhoen, M., Hocking, R. J., Atkins, C. J., Locksley, R. M., & Stockinger, B. (2006) · Immunity · doi:10.1016/j.immuni.2006.01.001 · Cited by 3,605 · cited 1×
“Accordingly, IL-1 is required for development of Th17 cell-sustained autoimmunity (e.g., Chung et al., 2009; Sutton et al., 2006; Veldhoen et al., 2006).”
Immunological and inflammatory functions of the interleukin-1 family
Dinarello, C. A. (2009) · Annual Review of Immunology · doi:10.1146/annurev.immunol.021908.132612 · Cited by 3,466 · cited 9×
“IL-1 affects virtually all cells and organs and is a major pathogenic mediator of autoinflammatory, autoimmune, infectious, and degenerative diseases (Dinarello, 2009, 2010; Dinarello et al., 2012; Gabay et al., 2010; Sims and Smith, 2010) (Table 2).”
InfluentialSelf-citationNeutrophils in the activation and regulation of innate and adaptive immunity
Mantovani, A., Cassatella, M. A., Costantini, C., & Jaillon, S. (2011) · Nature reviews. Immunology · doi:10.1038/nri3024 · Cited by 3,159 · cited 1×
“IL-1 markedly prolongs the lifespan and stimulates the effector function of neutrophils and macrophages (Mantovani et al., 2011).”
Non-canonical inflammasome activation targets caspase-11
Kayagaki, N., Warming, S., Lamkanfi, M., Walle, L. V., Louie, S., Dong, J., Newton, K., Qu, Y., Liu, J., Heldens, S., et al. (2011) · Nature · doi:10.1038/nature10558 · Cited by 2,530
Innate lymphoid cells — a proposal for uniform nomenclature
Spits, H., Artis, D., Colonna, M., Diefenbach, A., Disanto, J. D., Eberl, G., Koyasu, S., Locksley, R., McKenzie, A., Mebius, R., et al. (2013) · Nature reviews. Immunology · doi:10.1038/nri3365 · Cited by 2,380 · cited 4×
“The discovery of innate lymphoid cells and the dissection of pathways of T cell differentiation have revealed essential functions for IL-1, IL-18, and IL-33 and have opened vistas on their functions (O’Shea and Paul, 2010; Spits et al., 2013).”
InfluentialInterleukin-1 in the pathogenesis and treatment of inflammatory diseases
Dinarello, C. A. (2011) · Blood · doi:10.1182/blood-2010-07-273417 · Cited by 2,248 · cited 4×
“Extracellular cleavage of the inactive IL-1b precursor by neutrophil enzymes such a proteinase-3 and elastase generate active IL-1b because the cleavage site is close to that of caspase-1 (Dinarello, 2011).”
InfluentialNuocytes represent a new innate effector leukocyte that mediates type-2 immunity
Neill, D. R., Wong, S. H., Bellosi, A., Flynn, R. J., Daly, M. G., Langford, T. K. A., Bucks, C. M., Kane, C. M., Fallon, P. G., Pannell, R., et al. (2010) · Nature · doi:10.1038/nature08900 · Cited by 2,079 · cited 2×
“IL-33 plays a protective role against parasites ranging from nematode expulsion to control of Toxoplasma gondii encephalitis (Moro et al., 2010; Neill et al., 2010).”
A Large-Scale, Consortium-Based Genomewide Association Study of Asthma
Moffatt, M. F., Gut, I. G., Démenais, F., Strachan, D. P., Bouzigon, E., Heath, S. C., von Mutius, E., Farrall, M., Lathrop, M. G., & Cookson, W. (2010) · New England Journal of Medicine · doi:10.1056/nejmoa0906312 · Cited by 2,043 · cited 1×
“In humans, genome-wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) in the genes encoding ST2 and IL-33 associated with asthma (Moffatt et al., 2010).”
Innate production of TH2 cytokines by adipose tissue-associated c-Kit+Sca-1+ lymphoid cells
Moro, K., Yamada, T., Tanabe, M., Takeuchi, T., Ikawa, T., Kawamoto, H., Furusawa, J.-I., Ohtani, M., Fujii, H., & Koyasu, S. (2009) · Nature · doi:10.1038/nature08636 · Cited by 1,994 · cited 2×
“IL-33 plays a protective role against parasites ranging from nematode expulsion to control of Toxoplasma gondii encephalitis (Moro et al., 2010; Neill et al., 2010).”
Ghiringhelli, F., Apetoh, L., Tesniere, A., Aymeric, L., Ma, Y., Ortiz, C., Vermaelen, K., Panaretakis, T., Mignot, G., Ullrich, E., et al. (2009) · Nature Medicine · doi:10.1038/nm.2028 · Cited by 1,898 · cited 1×
“IL-1R1-deficient mice show defective capacity to generate effective CD8+ T cell responses to viruses (e.g., Joeckel et al., 2012) and tumors (Ghiringhelli et al., 2009).”
Phenotypic and functional features of human Th17 cells
Annunziato, F., Cosmi, L., Santarlasci, V., Maggi, L., Liotta, F., Mazzinghi, B., Parente, E., Filì, L., Ferri, S., Frosali, F., et al. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070663 · Cited by 1,861 · cited 1×
“Analysis of the differentiation of human naive T cells to Th17 cells originally revealed a key role of IL-1 (Acosta-Rodriguez et al., 2007; Annunziato et al., 2007).”
Acosta-Rodriguez, E. V., Napolitani, G., Lanzavecchia, A., & Sallusto, F. (2007) · Nature Immunology · doi:10.1038/ni1496 · Cited by 1,857
Treating inflammation by blocking interleukin-1 in a broad spectrum of diseases
Dinarello, C. A., Simon, A., & van der Meer, J. W. M. (2012) · Nature Reviews Drug Discovery · doi:10.1038/nrd3800 · Cited by 1,812 · cited 6×
“IL-1 affects virtually all cells and organs and is a major pathogenic mediator of autoinflammatory, autoimmune, infectious, and degenerative diseases (Dinarello, 2009, 2010; Dinarello et al., 2012; Gabay et al., 2010; Sims and Smith, 2010) (Table 2).”
InfluentialHoffman, H. M., Mueller, J. L., Broide, D. H., Wanderer, A. A., & Kolodner, R. D. (2001) · Nature Genetics · doi:10.1038/ng756 · Cited by 1,679
The IL-1 family: regulators of immunity
Sims, J. E., & Smith, D. E. (2010) · Nature reviews. Immunology · doi:10.1038/nri2691 · Cited by 1,459 · cited 17×
“IL-1 affects virtually all cells and organs and is a major pathogenic mediator of autoinflammatory, autoimmune, infectious, and degenerative diseases (Dinarello, 2009, 2010; Dinarello et al., 2012; Gabay et al., 2010; Sims and Smith, 2010) (Table 2).”
InfluentialMechanisms Underlying Lineage Commitment and Plasticity of Helper CD4 + T Cells
O’Shea, J. J., & Paul, W. E. (2010) · Science · doi:10.1126/science.1178334 · Cited by 1,401
Critical Regulation of Early Th17 Cell Differentiation by Interleukin-1 Signaling
Chung, Y., Chang, S. H., Martínez, G., Yang, X. O., Nurieva, R., Kang, H. S., Ma, L., Watowich, S. S., Jetten, A. M., Tian, Q., et al. (2009) · Immunity · doi:10.1016/j.immuni.2009.02.007 · Cited by 1,247 · cited 1×
“Accordingly, IL-1 is required for development of Th17 cell-sustained autoimmunity (e.g., Chung et al., 2009; Sutton et al., 2006; Veldhoen et al., 2006).”
IRAK (Pelle) Family Member IRAK-2 and MyD88 as Proximal Mediators of IL-1 Signaling
Muzio, M., Ni, J., Feng, P., & Dixit, V. M. (1997) · Science · doi:10.1126/science.278.5343.1612 · Cited by 1,170 · cited 7×
“Early on, it was realized that IL-1 was responsible for resistance against microbes (van der Meer et al., 1988), a discovery upstream of the identification of the TIR domain (originally standing for Toll-IL-1 resistance; shared by the IL-1 receptor [IL-1R] and Toll-like receptors [TLR]), and of the inflammasome.”
InfluentialAnti-inflammatory Agents: Present and Future
Dinarello, C. A. (2010) · Cell · doi:10.1016/j.cell.2010.02.043 · Cited by 1,095 · cited 18×
“IL-1 affects virtually all cells and organs and is a major pathogenic mediator of autoinflammatory, autoimmune, infectious, and degenerative diseases (Dinarello, 2009, 2010; Dinarello et al., 2012; Gabay et al., 2010; Sims and Smith, 2010) (Table 2).”
InfluentialSelf-citationIL-33 and ST2 comprise a critical biomechanically induced and cardioprotective signaling system
Sanada, S., Hakuno, D., Higgins, L., Schreiter, E. R., McKenzie, A. N. J., & Lee, R. T. (2007) · Journal of Clinical Investigation · doi:10.1172/jci30634 · Cited by 1,074 · cited 2×
“In cardiovascular diseasemodels, IL-33 plays a protective role by reducing atherosclerotic plaque formation (Miller et al., 2008) or by reducing cardiac hypertrophy secondary to pressure overload (Sanada et al., 2007).”
Sutton, C. E., Brereton, C. F., Keogh, B., Mills, K. H. G., & Lavelle, E. C. (2006) · The Journal of Experimental Medicine · doi:10.1084/jem.20060285 · Cited by 1,038 · cited 1×
“Accordingly, IL-1 is required for development of Th17 cell-sustained autoimmunity (e.g., Chung et al., 2009; Sutton et al., 2006; Veldhoen et al., 2006).”
Rodríguez-Prados, J.-C., Través, P. G., Cuenca, J., Rico, D., Aragonés, J., Martín-Sanz, P., Cascante, M., & Boscá, L. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.0901698 · Cited by 1,022 · cited 1×
“IL-1 is likely to orient macrophages to aerobic glycolysis as lipopolysaccharide (LPS) does (Rodrı́guez-Prados et al., 2010) and in turn it is downstream of metabolic responses elicited by microbial sensing.”
Disease-associated functions of IL-33: the new kid in the IL-1 family
Liew, F. Y., Pitman, N. I., & McInnes, I. B. (2010) · Nature reviews. Immunology · doi:10.1038/nri2692 · Cited by 1,020 · cited 2×
“IL-33 is a driver of type 2 inflammatory conditions such as asthma, fibrosis, and response to parasites (Liew et al., 2010; McHedlidze et al., 2013; Sica et al., 2013).”
Interleukin-36–Receptor Antagonist Deficiency and Generalized Pustular Psoriasis
Marrakchi, S., Guigue, P., Renshaw, B. R., Puel, A., Pei, X.-Y., Fraitag, S., Zribi, J., Bal, É., Cluzeau, C. V. M., Chrabieh, M., et al. (2011) · New England Journal of Medicine · doi:10.1056/nejmoa1013068 · Cited by 996 · cited 2×
“IL36RN (IL-36Ra, human) Severe psoriasis (Marrakchi et al., 2011)”
An Autoinflammatory Disease with Deficiency of the Interleukin-1–Receptor Antagonist
Aksentijevich, I. A., Masters, S. L., Ferguson, P. J., Dancey, P., Frenkel, J., van Royen‐Kerkhof, A., Laxer, R. M., Tedgård, U., Cowen, E. W., Pham, T., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0807865 · Cited by 981 · cited 1×
“Children bornwith a genetic deficiency of IL-1Ra or functional inactive IL-1Ra suffer from severe systemic and local inflammation, including pustular skin eruptions, vasculitis, osteolytic lesions, and sterile osteomyelitis (Aksentijevich et al., 2009; Reddy et al., 2009).”
Interleukin-1 Type II Receptor: A Decoy Target for IL-1 That Is Regulated by IL-4
Colotta, F., Re, F., Muzio, M., Bertini, R., Polentarutti, N., Sironi, M., Giri, J. G., Dower, S., Sims, J. E., & Mantovani, A. (1993) · Science · doi:10.1126/science.8332913 · Cited by 979 · cited 1×
“It has found that a subset of Th1 clones, in particular those characterized by expression of CD161, expresses IL1R1 (Cosmi et al., 2008; Maggi et al., 2012).”
Pathogen-induced human TH17 cells produce IFN-γ or IL-10 and are regulated by IL-1β
Zielinski, C. E., Mele, F., Aschenbrenner, D., Jarrossay, D., Ronchi, F., Gattorno, M., Monticelli, S., Lanzavecchia, A., & Sallusto, F. (2012) · Nature · doi:10.1038/nature10957 · Cited by 919 · cited 1×
“IL-1 also inhibits IL-10 production, which otherwise dampens IFN-g secretion (Zielinski et al., 2012).”
IL-1 pathways in inflammation and human diseases
Gabay, C., Lamacchia, C., & Palmer, G. (2010) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2010.4 · Cited by 897 · cited 8×
“IL-1 affects virtually all cells and organs and is a major pathogenic mediator of autoinflammatory, autoimmune, infectious, and degenerative diseases (Dinarello, 2009, 2010; Dinarello et al., 2012; Gabay et al., 2010; Sims and Smith, 2010) (Table 2).”
InfluentialChen, C.-J., Kono, H., Golenbock, D., Reed, G., Akira, S., & Rock, K. L. (2007) · Nature Medicine · doi:10.1038/nm1603 · Cited by 876 · cited 2×
“and colitis, reduced atherosclerosis (Chen et al., 2007; Krelin et al., 2007)”
Molofsky, A. B., Nussbaum, J. C., Liang, H.-E., Dyken, S. J. V., Cheng, L. E., Mohapatra, A., Chawla, A., & Locksley, R. M. (2013) · The Journal of Experimental Medicine · doi:10.1084/jem.20121964 · Cited by 867 · cited 2×
“IL-33 is also involved in inducing ILC2-dependent in- 1008 Immunity 39, December 12, 2013 ª2013 Elsevier Inc. creases in eosinophils and M2 polarized macrophages of visceral adipose tissue, which are implicated in metabolic homeostasis (Molofsky et al., 2013).”
IL-37 is a fundamental inhibitor of innate immunity
Nold, M. F., Nold‐Petry, C. A., Zepp, J. A., Palmer, B. E., Bufler, P., & Dinarello, C. A. (2010) · Nature Immunology · doi:10.1038/ni.1944 · Cited by 850
Interleukin-18 Binding Protein
Novick, D., Kim, S. H., Fantuzzi, G., Reznikov, L. L., Dinarello, C. A., & Rubinstein, M. (1999) · Immunity · doi:10.1016/s1074-7613(00)80013-8 · Cited by 781
Horai, R., Saijo, S., Tanioka, H., Nakae, S., Sudo, K., Okahara, A., Ikuse, T., Asano, M., & Iwakura, Y. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.191.2.313 · Cited by 752 · cited 1×
“Deficiency of IL-1Ra in mice results in spontaneous and lethal arteritis, destructive arthritis, and psoriatic-like skin lesions, as well as increased susceptibility to carcinogenesis (Horai et al., 2000; Nicklin et al., 2000).”
Kurowska‐Stolarska, M., Stolarski, B., Kewin, P., Murphy, G., Corrigan, C. J., Ying, S., Pitman, N. I., Mirchandani, A. S., Rana, B. M. J., van Rooijen, N., et al. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0901575 · Cited by 747
Human interleukin 17–producing cells originate from a CD161+CD4+ T cell precursor
Cosmi, L., Palma, R. D., Santarlasci, V., Maggi, L., Capone, M., Frosali, F., Rodolico, G., Querci, V., Abbate, G., Angeli, R., et al. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20080397 · Cited by 733 · cited 1×
“It has found that a subset of Th1 clones, in particular those characterized by expression of CD161, expresses IL1R1 (Cosmi et al., 2008; Maggi et al., 2012).”
The IL-1-like cytokine IL-33 is inactivated after maturation by caspase-1
Cayrol, C., & Girard, J.-P. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0812690106 · Cited by 707 · cited 1×
“IL-33 is inactivated by caspase-1 (Cayrol and Girard, 2009), and the 30 KDa protein is one of its bioactive forms.”
IL-33 is a crucial amplifier of innate rather than acquired immunity
Oboki, K., Ohno, T., Kajiwara, N., Arae, K., Morita, H., Ishii, A., Nambu, A., Abe, T., Kiyonari, H., Matsumoto, K., et al. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1003059107 · Cited by 670 · cited 1×
“IL-33 amplifies innate immunity and inflammatory responses, not necessarily dependent on the development of adaptive Th2 cell responses (Oboki et al., 2010).”
IL-33 reduces the development of atherosclerosis
Miller, A. M., Xu, D., Asquith, D. L., Denby, L., Li, Y., Sattar, N. A., Baker, A. H., McInnes, I. B., & Liew, F. Y. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20071868 · Cited by 642
IL-33 is processed into mature bioactive forms by neutrophil elastase and cathepsin G
Lefrançais, E., Roga, S., Gautier, V., de Peredo, A. G., Monsarrat, B., Girard, J., & Cayrol, C. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1115884109 · Cited by 631 · cited 1×
“As for other IL-1 familymembers, calpain and the neutrophil serine proteases cathepsin G and elastase cleave human IL-33 and generate more potent mature forms (Lefrançais et al., 2012).”
SIGIRR, a negative regulator of Toll-like receptor–interleukin 1 receptor signaling
Wald, D. N., Qin, J., Zhao, Z., Qian, Y., Naramura, M., Tian, L., Towne, J. E., Sims, J. E., Stark, G. R., & Li, X. (2003) · Nature Immunology · doi:10.1038/ni968 · Cited by 606 · cited 1×
“…following stimulation of IL-1R family members or TLRs (IL-1RI, IL-18R, ST2, TLR1, TLR2, TLR3, TLR4, TLR7, and TLR9) (Bulek et al., 2009; Garlanda et al., 2004; Lech et al., 2008; Wald et al., 2003), by interfering with the recruitment of TIR-containing adaptor molecules (Wald et al., 2003).”
The involvement of IL-1 in tumorigenesis, tumor invasiveness, metastasis and tumor-host interactions
Apte, R. N., Dotan, S., Elkabets, M., White, M. R., Reich, E., Carmi, Y., Song, X., Dvozkin, T., Krelin, Y., & Voronov, E. (2006) · Cancer and Metastasis Reviews · doi:10.1007/s10555-006-9004-4 · Cited by 589 · cited 2×
“Early observations on augmentation of metastasis by IL-1 were subsequently extended to primary carcinogenesis in different organs (Apte et al., 2006; Salcedo et al., 2013).”
Muzio, M., Natoli, G., Saccani, S., Levrero, M., & Mantovani, A. (1998) · The Journal of Experimental Medicine · doi:10.1084/jem.187.12.2097 · Cited by 573 · cited 7×
“Early on, it was realized that IL-1 was responsible for resistance against microbes (van der Meer et al., 1988), a discovery upstream of the identification of the TIR domain (originally standing for Toll-IL-1 resistance; shared by the IL-1 receptor [IL-1R] and Toll-like receptors [TLR]), and of the inflammasome.”
InfluentialIL-1α and IL-1β Recruit Different Myeloid Cells and Promote Different Stages of Sterile Inflammation
Rider, P., Carmi, Y., Guttman, O., Braiman, A., Cohen, I., Voronov, E., White, M. R., Dinarello, C. A., & Apte, R. N. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1102048 · Cited by 546
Dehghan, A., Dupuis, J., Barbalić, M., Bis, J. C., Eiríksdóttir, G., Lu, C., Pellikka, N., Wallaschofski, H., Kettunen, J., Henneman, P., et al. (2011) · Circulation · doi:10.1161/circulationaha.110.948570 · Cited by 507 · cited 1×
“In a GWAS of 66,185 subjects with elevated CRP, loci implicated in themetabolic syndrome include NLRP3, IL-6R, and IL-38 (Dehghan et al., 2011).”
Interleukin-33-Dependent Innate Lymphoid Cells Mediate Hepatic Fibrosis
Mchedlidze, T., Waldner, M., Zopf, S., Walker, J., Rankin, A. L., Schuchmann, M., Voehringer, D., McKenzie, A. N. J., Neurath, M. F., Pflanz, S., et al. (2013) · Immunity · doi:10.1016/j.immuni.2013.07.018 · Cited by 502
Interleukin-33 attenuates sepsis by enhancing neutrophil influx to the site of infection
Alves-Filho, J. C., Sônego, F., Souto, F. O., de Freitas, A., Verri, W. A., Jr., Auxiliadora‐Martins, M., Basile-Filho, A., McKenzie, A. N. J., Xu, D., Cunha, F. Q., et al. (2010) · Nature Medicine · doi:10.1038/nm.2156 · Cited by 485 · cited 1×
“In a murine model of sepsis, IL-33 has been found to enhance neutrophil recruitment to the site of infection and bacterial clearance by preventing TLR-mediated downregulation of the CXCR2 chemokine receptor (Alves-Filho et al., 2010).”
Doyle, S., Campbell, M., Ozaki, E., Salomon, R. G., Mori, A., Kenna, P. F., Farrar, G. J., Kiang, A., Humphries, M. M., Lavelle, E. C., et al. (2012) · Nature Medicine · doi:10.1038/nm.2717 · Cited by 428 · cited 1×
“In some models of disease as in age-related macular degeneration, IL-18 is protective (Doyle et al., 2012).”
Deficiency of interleukin-18 in mice leads to hyperphagia, obesity and insulin resistance
Netea, M. G., Joosten, L. A. B., Lewis, E., Jensen, D. R., Voshol, P. J., Kullberg, B. J., Tack, C. J., van Krieken, H., Kim, S.-H., Stalenhoef, A. F., et al. (2006) · Nature Medicine · doi:10.1038/nm1415 · Cited by 424 · cited 1×
“IL-18 and IL-18R-deficient aged mice spontaneously develop a metabolic syndrome similar to that of humans with diabetes, insulin resistance, and atherosclerosis (Netea et al., 2006).”
Self-citationIL-1 family members and STAT activators induce cytokine production by Th2, Th17, and Th1 cells
Guo, L., Wei, G., Zhu, J., Liao, W., Leonard, W. J., Zhao, K., & Paul, W. (2009) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0906988106 · Cited by 423 · cited 14×
“TIR8 inhibits NF-kB and JNK activation following stimulation of IL-1R family members or TLRs (IL-1RI, IL-18R, ST2, TLR1, TLR2, TLR3, TLR4, TLR7, and TLR9) (Bulek et al., 2009; Garlanda et al., 2004; Lech et al., 2008; Wald et al., 2003), by interfering with the recruitment of TIR-containing adaptor molecules (Wald et…”
InfluentialMacrophage Plasticity and Polarization in Liver Homeostasis and Pathology
Sica, A., Invernizzi, P., & Mantovani, A. (2014) · Hepatology · doi:10.1002/hep.26754 · Cited by 422 · cited 1×
“IL-33 is a driver of type 2 inflammatory conditions such as asthma, fibrosis, and response to parasites (Liew et al., 2010; McHedlidze et al., 2013; Sica et al., 2013).”
IL-1β-converting enzyme (caspase-1) in intestinal inflammation
Siegmund, B., Lehr, H.-A., Fantuzzi, G., & Dinarello, C. A. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.231473998 · Cited by 421 · cited 3×
“Induction of IFN-g by IL-18 requires caspase-1 processing (Siegmund et al., 2001b).”
Pecaric-Petkovic, T., Didichenko, S. A., Kämpfer, S. S., Spiegl, N., & Dahinden, C. A. (2008) · Blood · doi:10.1182/blood-2008-05-157818 · Cited by 420 · cited 1×
“By inducing IL-5 production in several cell types, ILCs in particular, and by promoting eosinophil maturation, IL-33 causes eosinophilia in vivo (Bouffi et al., 2013; Ikutani et al., 2012; Pecaric-Petkovic et al., 2009).”
An Autoinflammatory Disease Due to Homozygous Deletion of the IL1RN Locus
Reddy, S. T., Jia, S., Geoffrey, R., Lorier, R., Suchi, M., Broeckel, U., Hessner, M. J., & Verbsky, J. W. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0809568 · Cited by 408 · cited 1×
“Children bornwith a genetic deficiency of IL-1Ra or functional inactive IL-1Ra suffer from severe systemic and local inflammation, including pustular skin eruptions, vasculitis, osteolytic lesions, and sterile osteomyelitis (Aksentijevich et al., 2009; Reddy et al., 2009).”
Psoriasiform dermatitis is driven by IL-36–mediated DC-keratinocyte crosstalk
Tortola, L., Rosenwald, E., Abel, B., Blumberg, H., Schäfer, M., Coyle, A. J., Renauld, J., Werner, S., Kisielow, J., & Köpf, M. (2012) · Journal of Clinical Investigation · doi:10.1172/jci63451 · Cited by 408 · cited 2×
“IL-36a, IL-36b, IL-36g, and IL-36Ra do not contain caspase cleavage sites and N-terminal truncation at the level of the A-X-Asp motif conserved in all IL-1 family members dramatically increases their proinflammatory activity (Towne et al., 2011).”
ST2 as a Marker for Risk of Therapy-Resistant Graft-versus-Host Disease and Death
Lugt, M. T. V., Braun, T., Hanash, S., Ritz, J., Ho, V. T., Antin, J. H., Zhang, Q., Wong, C., Wang, H., Chin, A. P., et al. (2013) · New England Journal of Medicine · doi:10.1056/nejmoa1213299 · Cited by 403
van de Veerdonk, F. L., Stoeckman, A. K., Wu, G., Boeckermann, A. N., Azam, T., Netea, M. G., Joosten, L. A. B., van der Meer, J. W. M., Hao, R., Kalabokis, V., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1121534109 · Cited by 383 · cited 4×
“IL-38 binds to the extracellular domain of recombinant IL-1Rrp2 (IL-36R) expressed as an IgG1 fusion protein (van de Veerdonk et al., 2012).”
InfluentialPuren, A. J., Fantuzzi, G., & Dinarello, C. A. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.5.2256 · Cited by 379 · cited 1×
“Similar to IL-1a, the IL-18 precursor is found in nearly all the same mesenchymal cells in health in humans and mice (Puren et al., 1999), and IL-18 is associated with the monocyte membrane, as is IL-1a (Bellora et al., 2012).”
Dinarello, C. A., Arend, W. P., Sims, J. E., Smith, D. E., Blumberg, H., O'Neill, L. A. J., Goldbach‐Mansky, R. T., Pizarro, T. T., Hoffman, H. M., Bufler, P., et al. (2010) · Nature Immunology · doi:10.1038/ni1110-973 · Cited by 351 · cited 1×
“The IL-1 and IL-1R families have grown impressively in size, complexity, and division of labor (Dinarello et al., 2010, 2012; Dinarello, 2009, 2010;Gabay et al., 2010).”
Opposing activities of two novel members of the IL-1 ligand family regulate skin inflammation
Blumberg, H., Dinh, H., Trueblood, E. S., Pretorius, J. K., Kugler, D. G., Weng, N., Kanaly, S. T., Towne, J. E., Willis, C. R., Kuechle, M. K., et al. (2007) · The Journal of Experimental Medicine · doi:10.1084/jem.20070157 · Cited by 348 · cited 2×
“SLE, systemic lupus erythematosus; RA, rheumatoid arthritis; GvHD, graft versus host disease. inflammatory characteristics such as neutrophilia and elevated circulating concentrations of IL-1b and IL-18 and die in the neonatal period.”
Kim, S. H., Eisenstein, M., Reznikov, L. L., Fantuzzi, G., Novick, D., Rubinstein, M., & Dinarello, C. A. (2000) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.97.3.1190 · Cited by 342 · cited 1×
“By Immunity 39, December 12, 2013 ª2013 Elsevier Inc. 1011 preventing the binding of the agonist to IL-18R, and neutralizing IL-18 activity, IL-18BP dampens IFN-g production and consequently limits Th1 cell responses (Kim et al., 2000; Novick et al., 1999) (Figure 4).”
IL‐33‐activated dendritic cells are critical for allergic airway inflammation
Besnard, A., Togbe, D., Guillou, N., Erard, F., Quesniaux, V. F. J., & Ryffel, B. (2011) · European Journal of Immunology · doi:10.1002/eji.201041033 · Cited by 341 · cited 1×
“IL-33-activated dendritic cells (DCs) favor polarization of Th2 cells (Besnard et al., 2011).”
Cohen, I., Rider, P., Carmi, Y., Braiman, A., Dotan, S., White, M. R., Voronov, E., Martin, M. U., Dinarello, C. A., & Apte, R. N. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0915018107 · Cited by 340 · cited 2×
“The IL-1a precursor shuttles between the cytosol and nucleus with amazing rapidity (Cohen et al., 2010).”
Inflammasome-mediated disease animal models reveal roles for innate but not adaptive immunity
Brydges, S. D., Mueller, J. L., McGeough, M. D., Pena, C. A., Misaghi, A., Gandhi, C., Putnam, C. D., Boyle, D. L., Firestein, G. S., Horner, A. A., et al. (2009) · Immunity · doi:10.1016/j.immuni.2009.05.005 · Cited by 339
Long-term IL-33–producing epithelial progenitor cells in chronic obstructive lung disease
Byers, D. E., Alexander-Brett, J., Patel, A. C., Agapov, E., Dang-Vu, G., Jin, X., Wu, K., You, Y., Alevy, Y., Girard, J.-P., et al. (2013) · Journal of Clinical Investigation · doi:10.1172/jci65570 · Cited by 337 · cited 2×
“IL-13-dependent lung disease has been shown to depend on long-term epithelial progenitor cells programmed for excess IL-33 production (Byers et al., 2013).”
Xiao, H. Q., Gulen, M. F., Qin, J., Yao, J., Bulek, K., Kish, D. D., Altuntas, C. Z., Wald, D. N., Ma, C., Zhou, H., et al. (2007) · Immunity · doi:10.1016/j.immuni.2007.02.012 · Cited by 331
Towne, J. E., Renshaw, B. R., Douangpanya, J., Lipsky, B. P., Shen, M., Gabel, C. A., & Sims, J. E. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.267922 · Cited by 324 · cited 2×
“IL-36a, IL-36b, IL-36g, and IL-36Ra do not contain caspase cleavage sites and N-terminal truncation at the level of the A-X-Asp motif conserved in all IL-1 family members dramatically increases their proinflammatory activity (Towne et al., 2011).”
Interleukin 37 expression protects mice from colitis
McNamee, E. N., Masterson, J. C., Jedlicka, P., McManus, M. C., Grenz, A., Collins, C. B., Nold, M. F., Nold‐Petry, C. A., Bufler, P., Dinarello, C. A., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1111982108 · Cited by 320
Arterial Inflammation in Mice Lacking the Interleukin 1 Receptor Antagonist Gene
Nicklin, M. J. H., Hughes, D. E., Barton, J. L., Ure, J. M., & Duff, G. W. (2000) · The Journal of Experimental Medicine · doi:10.1084/jem.191.2.303 · Cited by 319 · cited 1×
“Deficiency of IL-1Ra in mice results in spontaneous and lethal arteritis, destructive arthritis, and psoriatic-like skin lesions, as well as increased susceptibility to carcinogenesis (Horai et al., 2000; Nicklin et al., 2000).”
Ikutani, M., Yanagibashi, T., Ogasawara, M., Tsuneyama, K., Yamamoto, S., Hattori, Y., Kouro, T., Itakura, A., Nagai, Y., Τακακι, S., et al. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1101270 · Cited by 314 · cited 1×
“By inducing IL-5 production in several cell types, ILCs in particular, and by promoting eosinophil maturation, IL-33 causes eosinophilia in vivo (Bouffi et al., 2013; Ikutani et al., 2012; Pecaric-Petkovic et al., 2009).”
Freigang, S., Ampenberger, F., Weiss, A., Kanneganti, T., Iwakura, Y., Hersberger, M., & Köpf, M. (2013) · Nature Immunology · doi:10.1038/ni.2704 · Cited by 313 · cited 1×
“Recent results have highlighted differential induction and role of IL-1a and IL-1b in fat induced vascular responses and atherosclerosis (Freigang et al., 2013).”
Pomerantz, B. J., Reznikov, L. L., Harken, A. H., & Dinarello, C. A. (2001) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.041611398 · Cited by 310 · cited 2×
“Similar to IL-1a, the IL-18 precursor is found in nearly all the same mesenchymal cells in health in humans and mice (Puren et al., 1999), and IL-18 is associated with the monocyte membrane, as is IL-1a (Bellora et al.”
IL-36R ligands are potent regulators of dendritic and T cells
Vigne, S., Palmer, G., Lamacchia, C., Martin, P., Talabot‐Ayer, D., Rodriguez, E., Ronchi, F., Sallusto, F., Dinh, H., Sims, J. E., et al. (2011) · Blood · doi:10.1182/blood-2011-05-356873 · Cited by 308 · cited 1×
“IL-36 is produced by innate immune cells and lymphocytes inducing the production of proinflammatory cytokines, chemokines, and costimulatory molecules, thus promoting Th1 and Th17 cell polarization (Vigne et al., 2011, 2012) (Figure 3B).”
Siegmund, B., Fantuzzi, G., Rieder, F., Gamboni-Robertson, F., Lehr, H.-A., Hartmann, G., Dinarello, C. A., Endres, S., & Eigler, A. (2001) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.2001.281.4.r1264 · Cited by 289 · cited 3×
“Induction of IFN-g by IL-18 requires caspase-1 processing (Siegmund et al., 2001b).”
Bossaller, L., Chiang, P.-I., Schmidt‐Lauber, C., Ganesan, S., Kaiser, W. J., Rathinam, V. A. K., Mocarski, E. S., Subramanian, D., Green, D. R., Silverman, N. S., et al. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1202121 · Cited by 287 · cited 1×
“By inducing IL-5 production in several cell types, ILCs in particular, and by promoting eosinophil maturation, IL-33 causes eosinophilia in vivo (Bouffi et al., 2013; Ikutani et al., 2012; Pecaric-Petkovic et al., 2009).”
Krelin, Y., Voronov, E., Dotan, S., Elkabets, M., Reich, E., Fogel, M., Huszar, M., Iwakura, Y., Segal, S., Dinarello, C. A., et al. (2007) · Cancer Research · doi:10.1158/0008-5472.can-06-2956 · Cited by 285 · cited 2×
“and colitis, reduced atherosclerosis (Chen et al., 2007; Krelin et al., 2007)”
IL-18–induced CD83+CCR7+NK helper cells
Mailliard, R. B., Alber, S. M., Shen, H., Watkins, S. C., Kirkwood, J. M., Herberman, R. B., & Kaliński, P. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20050128 · Cited by 285 · cited 1×
“IL-18 is a keymediator in the interaction between NK cells and DC or macrophages (e.g., Bellora et al., 2012; Mailliard et al., 2005).”
Kumar, S., Hanning, C. R., Brigham-Burke, M. R., Rieman, D. J., Lehr, R. V., Khandekar, S., Kirkpatrick, R. B., Scott, G. F., Lee, J. C., Lynch, F. J., et al. (2002) · Cytokine · doi:10.1006/cyto.2002.0873 · Cited by 260
Non-redundant properties of IL-1α and IL-1β during acute colon inflammation in mice
Bersudsky, M., Luski, L., Fishman, D., White, R. M., Ziv‐Sokolovskaya, N., Dotan, S., Rider, P., Kaplanov, I., Aychek, T., Dinarello, C. A., et al. (2013) · Gut · doi:10.1136/gutjnl-2012-303329 · Cited by 256
Intestinal inflammation in mice deficient in Tir8 , an inhibitory member of the IL-1 receptor family
Garlanda, C., Riva, F., Polentarutti, N., Buracchi, C., Sironi, M., Bortoli, M. D., Muzio, M., Bergottini, R., Scanziani, E., Vecchi, A., et al. (2004) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0308680101 · Cited by 254 · cited 1×
“…have shown that TIR8 plays nonredundant roles in regulating potentially detrimental inflammatory responses associated to infections, such as tuberculosis, candidiasis, aspergillosis, and P. aeruginosa infection (Bozza et al., 2008; Chen et al., 2011; Garlanda et al., 2007a; Huang et al., 2006).”
A complex of the IL-1 homologue IL-1F7b and IL-18-binding protein reduces IL-18 activity
Bufler, P., Azam, T., Gamboni-Robertson, F., Reznikov, L. L., Kumar, S., Dinarello, C. A., & Kim, S. (2002) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.212519099 · Cited by 252 · cited 2×
“Despite binding to the IL-18Ra chain, IL-37 does not act as a classical receptor antagonist (Bufler et al., 2002; Nold-Petry et al., 2009).”
The meta-analysis of genome-wide association studies
Thompson, J. R., Attia, J., & Minelli, C. (2011) · Briefings in Bioinformatics · doi:10.1093/bib/bbr020 · Cited by 251
Ben-Sasson, S. Z., Hogg, A. E., Hu‐Li, J., Wingfield, P. T., Chen, X., Crank, M. C., Caucheteux, S. M., Ratner, M., Berzofsky, J. A., Nir‐Paz, R., et al. (2013) · The Journal of Experimental Medicine · doi:10.1084/jem.20122006 · Cited by 249
van der Meer, J. W., Barza, M. J., Wolff, S. M., & Dinarello, C. A. (1988) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.85.5.1620 · Cited by 243 · cited 1×
“Early on, it was realized that IL-1 was responsible for resistance against microbes (van der Meer et al., 1988), a discovery upstream of the identification of the TIR domain (originally standing for Toll-IL-1 resistance; shared by the IL-1 receptor [IL-1R] and Toll-like receptors [TLR]), and of the…”
The IL-1 Family Member 7b Translocates to the Nucleus and Down-Regulates Proinflammatory Cytokines
Sharma, S., Kulk, N., Nold, M. F., Gräf, R., Kim, S., Reinhardt, D., Dinarello, C. A., & Bufler, P. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.180.8.5477 · Cited by 242 · cited 2×
“Gene databases do not contain a murine homolog for IL-37, but human IL-37 is functional in mouse cells (Bufler et al., 2002; Sharma et al., 2008).”
Sterile inflammation of endothelial cell-derived apoptotic bodies is mediated by interleukin-1α
Berda‐Haddad, Y., Robert, S., Salers, P., Zekraoui, L., Farnarier, C., Dinarello, C. A., Dignat‐George, F., & Kaplanski, G. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1116848108 · Cited by 240 · cited 1×
“However, circulating IL-1a is rarely detected even in persons with severe infections but is contained in apoptotic bodies released from endothelial cells (Berda-Haddad et al., 2011).”
Divergence of IL-1, IL-18, and cell death in NLRP3 inflammasomopathies
Brydges, S. D., Broderick, L., McGeough, M. D., Peña, C. A., Mueller, J. L., & Hoffman, H. M. (2013) · Journal of Clinical Investigation · doi:10.1172/jci71543 · Cited by 234
Duan, J., Chung, H., Troy, E. B., & Kasper, D. L. (2010) · Cell Host & Microbe · doi:10.1016/j.chom.2010.01.005 · Cited by 231 · cited 1×
“However, Tgd17 express the IL-1R and IL-1 in concert with IL-23 drives their activation and IL-1 production, thus setting in motion an amplification circuit (Duan et al., 2010; Zeng et al., 2012).”
Structural insights into the interaction of IL-33 with its receptors
Liu, X., Hammel, M., He, Y., Tainer, J. A., Jeng, U., Zhang, L., Wang, S., & Wang, X. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1308651110 · Cited by 223 · cited 1×
“The crystal structure of IL-33 in complex with the ectodomain of ST2 has recently been solved (Liu et al., 2013).”
Hughes, T. L., Becknell, B., Freud, A. G., McClory, S., Briercheck, E. L., Yu, J., Mao, C., Giovenzana, C., Nuovo, G. J., Wei, L., et al. (2010) · Immunity · doi:10.1016/j.immuni.2010.06.007 · Cited by 222 · cited 10×
“IL-38 does not bind to IL-1R1, IL-1R3, or to IL-18Rabut only to the IL-36R.”
InfluentialVigne, S., Palmer, G., Martin, P., Lamacchia, C., Strebel, D., Rodriguez, E., Olleros, M. L., Vesin, D., Garcia, I., Ronchi, F., et al. (2012) · Blood · doi:10.1182/blood-2012-06-439026 · Cited by 218
Palm, N. W., Rosenstein, R. K., Yu, S., Schenten, D., Florsheim, E. B., & Medzhitov, R. M. (2013) · Immunity · doi:10.1016/j.immuni.2013.10.006 · Cited by 217 · cited 3×
“The adaptive Th2 response against PLA2 is also IL-33 and ST2 dependent.”
Zeng, X., Wei, Y.-L., Huang, J., Newell, E. W., Yu, H., Kidd, B. A., Kuhns, M. S., Waters, R., Davis, M. M., Weaver, C. T., et al. (2012) · Immunity · doi:10.1016/j.immuni.2012.06.011 · Cited by 212 · cited 1×
“However, Tgd17 express the IL-1R and IL-1 in concert with IL-23 drives their activation and IL-1 production, thus setting in motion an amplification circuit (Duan et al., 2010; Zeng et al., 2012).”
The Role of IL-1β in the Early Tumor Cell–Induced Angiogenic Response
Carmi, Y., Dotan, S., Rider, P., Kaplanov, I., White, M. R., Baron, R., Abutbul, S., Huszar, M., Dinarello, C. A., Apte, R. N., et al. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1202769 · Cited by 212
Zheng, Y., Humphry, M., Maguire, J. J., Bennett, M. R., & Clarke, M. C. H. (2013) · Immunity · doi:10.1016/j.immuni.2013.01.008 · Cited by 205 · cited 2×
“Because IL-1R2 is expressed by a limited set of cells, this would represent a further mechanism of negative control of IL-1a by IL-1R2 during necrosis, restricted to specific cell types (Zheng et al., 2013).”
Gulen, M. F., Kang, Z., Bulek, K., Youzhong, W., Kim, T. W., Chen, Y., Altuntas, C. Z., Bak‐Jensen, K. S., McGeachy, M. J., Do, J., et al. (2010) · Immunity · doi:10.1016/j.immuni.2009.12.003 · Cited by 205
Paget, C., Ivanov, S., Fontaine, J., Renneson, J., Blanc, F., Pichavant, M., Dumoutier, L., Ryffel, B., Renauld, J., Gosset, P., et al. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.304758 · Cited by 199 · cited 1×
“IL-1, together with other cytokines, has been reported to induce IL-17 production by iNKT cells and, in the context of viral infection, IL-22 (Doisne et al., 2011; Monteiro et al., 2013; Paget et al., 2012).”
Inflammation links excess fat to insulin resistance: the role of the interleukin‐1 family
Tack, C. J., Stienstra, R., Joosten, L. A. B., & Netea, M. G. (2012) · Immunological Reviews · doi:10.1111/j.1600-065x.2012.01145.x · Cited by 199 · cited 1×
“IL-1 production can be a consequence of alterations in the homeostatic metabolic state as observed in obesity (dysbiosis) (Tack et al., 2012) (Figure 2A).”
Smith, D. E., Hanna, R., Friend, D. J., Moore, H. M., Chen, H., Farese, A. M., MacVittie, T. J., Virca, G. D., & Sims, J. E. (2003) · Immunity · doi:10.1016/s1074-7613(02)00514-9 · Cited by 185 · cited 1×
“Finally, soluble IL-1R2 and soluble IL-1RAcP bind pro-IL-1bwith high affinity and block its processing by caspase-1 (Smith et al., 2003).”
Bulek, K., Swaidani, S., Qin, J., Lu, Y., Gulen, M. F., Herjan, T., Min, B., Kastelein, R. A., Aronica, M. A., Kosz‐Vnenchak, M., et al. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0802729 · Cited by 178
Garlanda, C., Anders, H., & Mantovani, A. (2009) · Trends in Immunology · doi:10.1016/j.it.2009.06.001 · Cited by 169 · cited 1×
“TIR8 is expressed in several tissues, particularly in the kidney, digestive tract, liver, lung, and lymphoid organs (Garlanda et al., 2009).”
Structural insights into the assembly and activation of IL-1β with its receptors
Wang, D., Zhang, S., Li, L., Liu, X., Mei, K., & Wang, X. (2010) · Nature Immunology · doi:10.1038/ni.1925 · Cited by 162 · cited 1×
“The overall structure of the IL-1b-IL-1R2-IL-1RAcP complex is similar to that of the signaling ligand-receptor complex (Wang et al., 2010).”
Espinassous, Q., Paco, E. G. D., García-Verdugo, I., Synguélakis, M., von Aulock, S., Sallenave, J., McKenzie, A. N. J., & Kanellopoulos, J. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0803067 · Cited by 158 · cited 1×
“In macrophages, IL-33 favors LPS-dependent cytokine and chemokine production, and M2 macrophage polarization (Espinassous et al., 2009; KurowskaStolarska et al., 2009).”
IL-1 and T Helper Immune Responses
Santarlasci, V., Cosmi, L., Maggi, L., Liotta, F., & Annunziato, F. (2013) · Frontiers in Immunology · doi:10.3389/fimmu.2013.00182 · Cited by 148 · cited 1×
“It is therefore not surprising that IL-18 has been associated with Th1 cell differentiation (Santarlasci et al., 2013).”
Croonian Lecture, 1906.—On nerve endings and on special excitable substances in cells
Langley, J. N. (1906) · Proceedings of the Royal Society of London Series B Containing Papers of a Biological Character · doi:10.1098/rspb.1906.0056 · Cited by 146 · cited 1×
“The IL-1R2 receptor was identified as a decoy for IL-1 (Colotta et al., 1993), a paradigm shift since the original definition of ‘‘receptor’’ by Langley in the 19th century (Langley, 1906).”
Doisne, J., Soulard, V., Bécourt, C., Amniai, L., Henrot, P., Havenar‐Daughton, C., Blanchet, C., Zitvogel, L., Ryffel, B., Cavaillon, J., et al. (2010) · The Journal of Immunology · doi:10.4049/jimmunol.1002725 · Cited by 143
Zhao, J., Wei, J., Mialki, R. K., Mallampalli, D., Chen, B. B., Coon, T. A., Zou, C., Mallampalli, R. K., & Zhao, Y. (2012) · Nature Immunology · doi:10.1038/ni.2341 · Cited by 142
Distinctive features of classic and nonclassic ( T h17 derived) human T h1 cells
Maggi, L., Santarlasci, V., Capone, M., Rossi, M. C., Querci, V., Mazzoni, A., Cimaz, R., Palma, R. D., Liotta, F., Maggi, E., et al. (2012) · European Journal of Immunology · doi:10.1002/eji.201242648 · Cited by 140 · cited 1×
“It has found that a subset of Th1 clones, in particular those characterized by expression of CD161, expresses IL1R1 (Cosmi et al., 2008; Maggi et al., 2012).”
Albacker, L. A., Chaudhary, V., Chang, Y.-J., Kim, H. Y., Chuang, Y.-T., Pichavant, M., DeKruyff, R. H., Savage, P. B., & Umetsu, D. T. (2013) · Nature Medicine · doi:10.1038/nm.3321 · Cited by 140
The natural and the inducible: interleukin (IL)-17-producing γδ T cells
Chien, Y., Zeng, X., & Prinz, I. (2012) · Trends in Immunology · doi:10.1016/j.it.2012.11.004 · Cited by 139 · cited 1×
“Immunity 39, December 12, 2013 ª2013 Elsevier Inc. 1013 Tgdcells are themajor sourceof IL-17earlyafter infection (Chien et al., 2013).”
Myles, I. A., Fontecilla, N. M., Valdez, P. A., Vithayathil, P. J., Naik, S., Belkaid, Y., Ouyang, W., & Datta, S. K. (2013) · Nature Immunology · doi:10.1038/ni.2637 · Cited by 136 · cited 1×
“In a mouse model of skin infection, resistance to S. aureus depends on IL-1, which promotes IL-17 production by Tgd cells (Myles et al., 2013).”
Smith, D. E., Lipsky, B. P., Russell, C. B., Ketchem, R. R., Kirchner, J., Hensley, K. M., Huang, Y., Friedman, W., Boissonneault, V., Plante, M.-M., et al. (2009) · Immunity · doi:10.1016/j.immuni.2009.03.020 · Cited by 135 · cited 15×
“Moreover, IL-1R2 forms a complex with IL-1 and the IL-1RAcP, exerting a dominant-negative effect.”
InfluentialSakai, N., Sweringen, H. L. V., Belizaire, R. M., Quillin, R. C., Schuster, R. M., Blanchard, J. A., Burns, J. M., Tevar, A. D., Edwards, M. J., & Lentsch, A. B. (2012) · Journal of Gastroenterology and Hepatology · doi:10.1111/j.1440-1746.2012.07187.x · Cited by 132 · cited 1×
“IL-37Tg mice are protected against inflammatory conditions involving the gut (DSS-induced colitis) (McNamee et al., 2011), the heart (ischemic heart injury) (Yousif et al., 2011), and the liver (ischemia and reperfusion) (Sakai et al., 2012).”
Association between the interleukin‐1 family gene cluster and psoriatic arthritis
Rahman, P., Sun, S., Peddle, L., Snelgrove, T., Melay, W., Greenwood, C. M. T., & Gladman, D. D. (2006) · Arthritis & Rheumatism · doi:10.1002/art.21928 · Cited by 131
Garlanda, C., Riva, F., Veliz, T., Polentarutti, N., Pasqualini, F., Radaelli, E., Sironi, M., Nebuloni, M., Zorini, E. O., Scanziani, E., et al. (2007) · Cancer Research · doi:10.1158/0008-5472.can-07-0560 · Cited by 125 · cited 1×
“TIR8 is expressed in several tissues, particularly in the kidney, digestive tract, liver, lung, and lymphoid organs (Garlanda et al., 2009).”
Common genetic variation at the IL1RL1 locus regulates IL-33/ST2 signaling
Ho, J. E., Chen, W., Chen, M., Larson, M. G., McCabe, E. L., Cheng, S. C., Ghorbani, A., Coglianese, E. E., Emilsson, V., Johnson, A. D., et al. (2013) · Journal of Clinical Investigation · doi:10.1172/jci67119 · Cited by 124 · cited 14×
“TIR8 inhibits NF-kB and JNK activation following stimulation of IL-1R family members or TLRs (IL-1RI, IL-18R, ST2, TLR1, TLR2, TLR3, TLR4, TLR7, and TLR9) (Bulek et al., 2009; Garlanda et al., 2004; Lech et al., 2008; Wald et al., 2003), by interfering with the recruitment of TIR-containing adaptor molecules (Wald et…”
InfluentialLack of Toll IL-1R8 Exacerbates Th17 Cell Responses in Fungal Infection
Bozza, S., Zelante, T., Moretti, S., Bonifazi, P., DeLuca, A., D’Angelo, C., Giovannini, G., Garlanda, C., Boon, L., Bistoni, F., et al. (2008) · The Journal of Immunology · doi:10.4049/jimmunol.180.6.4022 · Cited by 120 · cited 2×
“aeruginosa infection (Bozza et al., 2008; Chen et al., 2011; Garlanda et al., 2007a; Huang et al., 2006).”
Regulated Intramembrane Proteolysis of the Interleukin-1 Receptor II by α-, β-, and γ-Secretase
Kuhn, P.-H., Marjaux, E., Imhof, A., De Strooper, B., Haass, C., & Lichtenthaler, S. F. (2007) · Journal of Biological Chemistry · doi:10.1074/jbc.m700356200 · Cited by 120 · cited 1×
“It is released in a soluble form (Kuhn et al., 2007; Lorenzen et al., 2012) as a consequence of proteolytic processing or alternative splicing.”
Garlanda, C., Liberto, D. D., Vecchi, A., Manna, M. P. L., Buracchi, C., Caccamo, N., Salerno, A., Dieli, F., & Mantovani, A. (2007) · The Journal of Immunology · doi:10.4049/jimmunol.179.5.3119 · Cited by 119
IL-1β suppresses innate IL-25 and IL-33 production and maintains helminth chronicity
Zaiss, M. M., Maslowski, K. M., Mosconi, I., Guenat, N., Marsland, B. J., & Harris, N. L. (2013) · PLoS Pathogens · doi:10.1371/journal.ppat.1003531 · Cited by 116 · cited 1×
“Interestingly, IL-1b suppresses IL-25 and IL-33 production maintaining chronicity of helminthic infection (Zaiss et al., 2013).”
Tir8/Sigirr prevents murine lupus by suppressing the immunostimulatory effects of lupus autoantigens
Lech, M., Kulkarni, O. P., Pfeiffer, S., Savarese, E., Krug, A., Garlanda, C., Mantovani, A., & Anders, H. (2008) · The Journal of Experimental Medicine · doi:10.1084/jem.20072646 · Cited by 116 · cited 4×
“…also associated with increased susceptibility to develop allergy and autoimmunity in various models including systemic lupus erythematosus, lupus nephritis (Lech et al., 2008, 2010), arthritis (Drexler et al., 2010), experimental autoimmune encephalomyelitis, and psoriasis (Russell et al., 2013).”
InfluentialThe IL ‐36 receptor pathway regulates A spergillus fumigatus‐induced T h1 and T h17 responses
Gresnigt, M. S., Rösler, B., Jacobs, C. W. M., Becker, K. L., Joosten, L. A. B., van der Meer, J. W. M., Netea, M. G., Dinarello, C. A., & van de Veerdonk, F. L. (2012) · European Journal of Immunology · doi:10.1002/eji.201242711 · Cited by 112
Bouffi, C., Rochman, M., Zust, C. B., Stucke, E. M., Kartashov, A. V., Fulkerson, P. C., Barski, A., & Rothenberg, M. E. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1301465 · Cited by 106 · cited 1×
“By inducing IL-5 production in several cell types, ILCs in particular, and by promoting eosinophil maturation, IL-33 causes eosinophilia in vivo (Bouffi et al., 2013; Ikutani et al., 2012; Pecaric-Petkovic et al., 2009).”
Re, F., Sironi, M., Muzio, M., Matteucci, C., Introna, M., Orlando, S., Pentón‐Rol, G., Dower, S., Sims, J. E., Colotta, F., et al. (1996) · The Journal of Experimental Medicine · doi:10.1084/jem.183.4.1841 · Cited by 102
MyD88 and its divergent toll in carcinogenesis
Salcedo, R., Cataisson, C., Hasan, U. A., Yuspa, S. H., & Trinchieri, G. (2013) · Trends in Immunology · doi:10.1016/j.it.2013.03.008 · Cited by 100 · cited 3×
“Early observations on augmentation of metastasis by IL-1 were subsequently extended to primary carcinogenesis in different organs (Apte et al., 2006; Salcedo et al., 2013).”
Macrophage-Derived IL-33 Is a Critical Factor for Placental Growth
Fock, V., Mairhofer, M., Otti, G. R., Hiden, U., Spittler, A., Zeisler, H., Fiala, C., Knöfler, M., & Pollheimer, J. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1300490 · Cited by 96 · cited 1×
“Macrophage-derived IL-33 has been shown to be a regulator of trophoblast proliferation and placental growth during early pregnancy (Fock et al., 2013).”
Novick, D., Elbirt, D., Miller, G., Dinarello, C. A., Rubinstein, M., & Sthoeger, Z. M. (2009) · Journal of Autoimmunity · doi:10.1016/j.jaut.2009.08.002 · Cited by 95 · cited 1×
“In several IFN-gmediated autoimmune conditions, the concentrations of free IL-18 compared to IL-18 bound to IL-18BP is important in determining the severity of the disease (Novick et al., 2010).”
Lech, M., Avila‐Ferrufino, A., Allam, R., Segerer, S., Khandoga, A. G., Krombach, F., Garlanda, C., Mantovani, A., & Anders, H. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0900118 · Cited by 93 · cited 1×
“TIR8 is expressed in several tissues, particularly in the kidney, digestive tract, liver, lung, and lymphoid organs (Garlanda et al., 2009).”
Bellora, F., Castriconi, R., Doni, A., Cantoni, C., Moretta, L., Mantovani, A., Moretta, A., & Bottino, C. (2012) · European Journal of Immunology · doi:10.1002/eji.201142173 · Cited by 92 · cited 2×
“Similar to IL-1a, the IL-18 precursor is found in nearly all the same mesenchymal cells in health in humans and mice (Puren et al., 1999), and IL-18 is associated with the monocyte membrane, as is IL-1a (Bellora et al., 2012).”
IL-33–dependent induction of allergic lung inflammation by FcγRIII signaling
Tjota, M. Y., Williams, J. W., Lu, T., Clay, B. S., Byrd, T. T., Hrusch, C. L., Decker, D. C., de Araujo, C. A., Bryce, P. J., & Sperling, A. I. (2013) · Journal of Clinical Investigation · doi:10.1172/jci63802 · Cited by 84 · cited 2×
“fumigatus-induced airway hyperreactivity (Albacker et al., 2013; Tjota et al., 2013).”
Huang, X., Hazlett, L. D., Du, W., & Barrett, R. P. (2006) · The Journal of Immunology · doi:10.4049/jimmunol.177.1.548 · Cited by 81 · cited 1×
“…have shown that TIR8 plays nonredundant roles in regulating potentially detrimental inflammatory responses associated to infections, such as tuberculosis, candidiasis, aspergillosis, and P. aeruginosa infection (Bozza et al., 2008; Chen et al., 2011; Garlanda et al., 2007a; Huang et al., 2006).”
Expression and Function of TNF and IL-1 Receptors on Human Regulatory T Cells
Mercer, F. K., Kozhaya, L., & Unutmaz, D. (2010) · PLoS ONE · doi:10.1371/journal.pone.0008639 · Cited by 80 · cited 1×
“…is expressed by a large variety of cell types, IL-1R2 is expressed by amore limited set of cell types, including monocytes, polarized M2 macrophages, microglial cells, neutrophils, B cells, and T regulatory (Treg) cells (Colotta et al., 1993;Martin et al., 2013;Mercer et al., 2010; Reet al., 1996).”
Induced IL-17–Producing Invariant NKT Cells Require Activation in Presence of TGF-β and IL-1β
Monteiro, M., Almeida, C. F., Agua‐Doce, A., & Graça, L. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1201010 · Cited by 77 · cited 7×
“IL-18, together with IL15, is a major stimulus for IFN-g production by group 1 ILCs; IL-33, acting in synergy with IL-25, is a potent inducer of the expansion of type 2 ILCs and of the production of extremely high amounts of Th2 cell-associated cytokines, in particular IL5 and IL-13; IL-1b and IL-23 activate group 3 I…”
InfluentialGrimsby, S., Jaensson, H., Dubrovska, A., Lomnytska, M. I., Hellman, U., & Souchelnytskyi, S. (2004) · FEBS Letters · doi:10.1016/j.febslet.2004.09.069 · Cited by 76 · cited 1×
“The nuclear translocation and anti-inflammatory properties of IL-37 appear to be linked to binding to the Smad3 (Grimsby et al., 2004) transcription factor for the antiinflammatory and immunosuppressive properties of TGF-b.”
Maksymowych, W. P., Rahman, P., REEVE, J. P., Gladman, D. D., Peddle, L., & Inman, R. D. (2006) · Arthritis & Rheumatism · doi:10.1002/art.21642 · Cited by 74 · cited 1×
“Allele combinations that include IL-38 polymorphisms are associated with psoriatic arthritis and ankylosing spondylitis (Maksymowych et al., 2006; Rahman et al., 2006), suggesting that IL-38 plays an important role in the pathogenesis of these inflammatory diseases.”
Lorenzen, I., Lokau, J., Düsterhöft, S., Trad, A., Garbers, C., Scheller, J., Rose‐John, S., & Grötzinger, J. (2012) · FEBS Letters · doi:10.1016/j.febslet.2012.03.012 · Cited by 72 · cited 1×
“It is released in a soluble form (Kuhn et al., 2007; Lorenzen et al., 2012) as a consequence of proteolytic processing or alternative splicing.”
Drexler, S. K., Kong, P. L., Inglis, J. J., Williams, R. O., Garlanda, C., Mantovani, A., Yazdi, A. S., Brennan, F. M., Feldmann, M., & Foxwell, B. M. J. (2010) · Arthritis & Rheumatism · doi:10.1002/art.27517 · Cited by 70 · cited 2×
“…also associated with increased susceptibility to develop allergy and autoimmunity in various models including systemic lupus erythematosus, lupus nephritis (Lech et al., 2008, 2010), arthritis (Drexler et al., 2010), experimental autoimmune encephalomyelitis, and psoriasis (Russell et al., 2013).”
Martin, P., Palmer, G., Vigne, S., Lamacchia, C., Rodriguez, E., Talabot‐Ayer, D., Rose‐John, S., Chalaris, A., & Gabay, C. (2013) · Journal of Leukocyte Biology · doi:10.1189/jlb.0113035 · Cited by 67 · cited 2×
“cell types, IL-1R2 is expressed by amore limited set of cell types, including monocytes, polarized M2 macrophages, microglial cells, neutrophils, B cells, and T regulatory (Treg) cells (Colotta et al., 1993;Martin et al., 2013;Mercer et al., 2010; Reet al., 1996).”
Lack of SIGIRR/TIR8 aggravates hydrocarbon oil‐induced lupus nephritis
Lech, M., Skuginna, V., Kulkarni, O. P., Gong, J., Wei, T., Stark, R. W., Garlanda, C., Mantovani, A., & Anders, H. (2009) · The Journal of Pathology · doi:10.1002/path.2678 · Cited by 60 · cited 1×
“…also associated with increased susceptibility to develop allergy and autoimmunity in various models including systemic lupus erythematosus, lupus nephritis (Lech et al., 2008, 2010), arthritis (Drexler et al., 2010), experimental autoimmune encephalomyelitis, and psoriasis (Russell et al., 2013).”
Xiao, H. Q., Yin, W., Ma, K., Gulen, M. F., Zhou, H., Sham, H. P., Jacobson, K., Vallance, B. A., & Li, X. (2010) · Gastroenterology · doi:10.1053/j.gastro.2010.04.043 · Cited by 60 · cited 2×
“TIR8 can also regulate mTOR kinase activity in Th17 lymphocytes (Gulen et al., 2010) and in intestinal epithelial cells (Xiao et al., 2010).”
The Toll-IL-1R Member Tir8/SIGIRR Negatively Regulates Adaptive Immunity against Kidney Grafts
Noris, M., Cassis, P., Azzollini, N., Cavinato, R. A., Cugini, D., Casiraghi, F., Aiello, S., Solini, S., Cassis, L., Mister, M., et al. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0803549 · Cited by 56 · cited 1×
“In kidney ischemia or transplantation, TIR8-deficiency causes increased renal injury or severe graft rejection, associated with excessive inflammation and amplified adaptive immune responses against donor antigens (Lech et al., 2009; Noris et al., 2009).”
Lack of TIR8/SIGIRR triggers progression of chronic lymphocytic leukemia in mouse models
Bertilaccio, M. T. S., Simonetti, G., Dagklis, A., Rocchi, M., Rodríguez, T. V., Apollonio, B., Mantovani, A., Ponzoni, M., Ghia, P., Garlanda, C., et al. (2011) · Blood · doi:10.1182/blood-2011-01-329870 · Cited by 53
Nold‐Petry, C. A., Nold, M. F., Nielsen, J. W., Bustamante, A., Zepp, J. A., Storm, K., Hong, J., Kim, S., & Dinarello, C. A. (2009) · Journal of Biological Chemistry · doi:10.1074/jbc.m109.004184 · Cited by 43 · cited 1×
“Despite binding to the IL-18Ra chain, IL-37 does not act as a classical receptor antagonist (Bufler et al., 2002; Nold-Petry et al., 2009).”
Russell, S. E., Stefanska, A. M., Kubica, M., Horan, R. M., Mantovani, A., Garlanda, C., Fallon, P. G., & Walsh, P. T. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1300828 · Cited by 40 · cited 3×
“…also associated with increased susceptibility to develop allergy and autoimmunity in various models including systemic lupus erythematosus, lupus nephritis (Lech et al., 2008, 2010), arthritis (Drexler et al., 2010), experimental autoimmune encephalomyelitis, and psoriasis (Russell et al., 2013).”
Chen, X., Zhao, Y., Wu, X., & Qian, G. (2010) · Shock · doi:10.1097/shk.0b013e3181f226f3 · Cited by 24 · cited 1×
“…have shown that TIR8 plays nonredundant roles in regulating potentially detrimental inflammatory responses associated to infections, such as tuberculosis, candidiasis, aspergillosis, and P. aeruginosa infection (Bozza et al., 2008; Chen et al., 2011; Garlanda et al., 2007a; Huang et al., 2006).”
Joeckel, L. T., Wallich, R., Metkar, S. S., Froelich, C. J., Simon, M. M., & Borner, C. (2012) · Journal of Virology · doi:10.1128/jvi.00682-12 · Cited by 22 · cited 1×
“IL-1R1-deficient mice show defective capacity to generate effective CD8+ T cell responses to viruses (e.g., Joeckel et al., 2012) and tumors (Ghiringhelli et al., 2009).”
Nold, M. F., Nold‐Petry, C. A., Lo, C. Y.-W., Li, S., Rudloff, I., Zepp, J. A., Azam, T., Bufler, P., Garlanda, C., Mantovani, A., et al. (2013) · Cytokine · doi:10.1016/j.cyto.2013.06.190 · Cited by 11 · cited 2×
“Available evidence suggests that IL-37 engages the IL-18Ra to deliver an inhibitory signal by using TIR8 (Nold et al., 2013).”
MethodLuo, Y., Cai, X., Liu, S., Wang, S., Nold‐Petry, C. A., Nold, M. F., Bufler, P., Norris, D. A., Dinarello, C. A., & Fujita, M. (2013) · Cytokine · doi:10.1016/j.cyto.2013.06.174 · Cited by 8 · cited 1×
“In addition, there is evidence that IL-37 expressing DCs have defective capacity to activate effective T cell responses and induce T regulatory cells (Luo et al., 2013).”
Hong, D. S., Naing, A., Falchook, G. S., Piha-Paul, S. A., Wheler, J. J., Fu, S., Tsimberidou, A. M., Hui, D., Scott, R., Khan, R. S., et al. (2011) · Molecular Cancer Therapeutics · doi:10.1158/1535-7163.targ-11-a211 · Cited by 6 · cited 2×
“A neutralizing monoclonal anti-IL-1a antibody has been tested in Type 2 diabetes, cancer cachexia, pustular psoriasis, occlusive vascular disease, and scarring acne vulgaris and in each condition, reduced disease severity has been observed in limited trials (Hong et al., 2011).”
Research works printed but not linked: 1
- Yousif, 2011, Expression of IL-37 in mouse protects the myocardium against ischemic injury via modulation of NF-κB activation, Circulation, 124, A8603
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“These pyrogens are produced as cytosolic factors that lack an N-terminal secretion signal, and are therefore not released from cells via the conventional secretory pathway (Garlanda et al., 2013).”
InfluentialCytokine release syndrome and associated neurotoxicity in cancer immunotherapy
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Metadata
- Authors
- Garlanda, C., Dinarello, C. A., & Mantovani, A.
- Affiliations
- Radboud University Medical Center (NL)
- University of Milan (IT)
- Corresponding author
- Mantovani, Alberto
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 39
- Issue
- 6
- Pages
- 1003-1018
- ISSN
- 1074-7613 (ISSN-L)
- PMC
- PMC3933951
- OpenAlex
- W2145866317
- Cited by
- 1,945
- References
- 151
- Citations by year
- 2026: 80 · 2025: 118 · 2024: 136 · 2023: 122 · 2022: 168 · 2021: 172 · 2020: 202 · 2019: 165 · 2018: 194 · 2017: 192 · 2016: 171 · 2015: 156 · 2014: 66 · 2013: 1
- FWCI
- 11.46
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Radboud Repository (Radboud University) (submittedVersion)
- Funders
- European Research Council
- Associazione Italiana per la Ricerca sul Cancro
- National Institutes of Health (A115614, AR-45584)
- European Commission (FP7-HEALTH-2011- ADITEC 280873)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › IL-33, ST2, and ILC Pathways
- Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Keywords
- interleukin-1 family, innate immunity, inflammation, IL-1 receptor family, interleukin-1 receptor antagonist, decoy receptor, IL-18, IL-33, IL-36, IL-37, IL-38, IL1RAP, SIGIRR, negative regulation of cytokine signaling, lymphocyte differentiation, innate and adaptive immunity
- MeSH terms
- Animals, Gene Expression Regulation, Humans, Immunity, Innate, Interleukin-1, Interleukins, Ligands, Receptors, Interleukin-1, Adaptive Immunity
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