Cited by 1,191Multiple Sclerosis Research StudiesPsoriasis: Treatment and PathogenesisT-cell and B-cell Immunology

The DOI matches its Crossref record; 44 of the 44 references it cites were found in a registry or an index.

RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation

Codarri, Laura, Gyülvészi, Gabor, Tosevski, Vinko, Hesske, Lysann, Fontana, Adriano, Magnenat, Laurent, Suter, Tobias, Becher, Burkhard·2011·Nature Immunology

DOI 10.1038/ni.2027

Open this paper in CoChat — free account

Abstract

Although the role of the T(H)1 and T(H)17 subsets of helper T cells as disease mediators in autoimmune neuroinflammation remains a subject of some debate, none of their signature cytokines are essential for disease development. Here we report that interleukin 23 (IL-23) and the transcription factor RORγt drove expression of the cytokine GM-CSF in helper T cells, whereas IL-12, interferon-γ (IFN-γ) and IL-27 acted as negative regulators. Autoreactive helper T cells specifically lacking GM-CSF failed to initiate neuroinflammation despite expression of IL-17A or IFN-γ, whereas GM-CSF secretion by Ifng(-/-)Il17a(-/-) helper T cells was sufficient to induce experimental autoimmune encephalomyelitis (EAE). During the disease effector phase, GM-CSF sustained neuroinflammation via myeloid cells that infiltrated the central nervous system. Thus, in contrast to all other known helper T cell-derived cytokines, GM-CSF serves a nonredundant function in the initiation of autoimmune inflammation regardless of helper T cell polarization.

Integrity signals

Registry

Crossref · 10.1038/ni.2027

Cites

44 of 44 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells
Bettelli, E., Carrier, Y., Gao, W., Korn, T., Strom, T. B., Oukka, M., Weiner, H. L., & Kuchroo, V. K. (2006) · Nature · doi:10.1038/nature04753 · Cited by 6,992
The Orphan Nuclear Receptor RORγt Directs the Differentiation Program of Proinflammatory IL-17+ T Helper Cells
Ivanov, I. I., McKenzie, B. S., Zhou, L., Tadokoro, C. E., Lepelley, A., Lafaille, J. J., Cua, D. J., & Littman, D. R. (2006) · Cell · doi:10.1016/j.cell.2006.07.035 · Cited by 5,145
Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages
Harrington, L. E., Hatton, R. D., Mangan, P. R., Turner, H., Murphy, T. L., Murphy, K. M., & Weaver, C. T. (2005) · Nature Immunology · doi:10.1038/ni1254 · Cited by 4,742
A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17
Park, H., Li, Z., Yang, X. O., Chang, S. H., Nurieva, R., Wang, Y.-H., Wang, Y., Hood, L., Zhu, Z., Tian, Q., et al. (2005) · Nature Immunology · doi:10.1038/ni1261 · Cited by 4,265
IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
Langrish, C. L., Chen, Y., Blumenschein, W. M., Mattson, J., Basham, B., Sedgwick, J. D., McClanahan, T., Kastelein, R. A., & Cua, D. J. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041257 · Cited by 4,099
TGFβ in the Context of an Inflammatory Cytokine Milieu Supports De Novo Differentiation of IL-17-Producing T Cells
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
Interleukin-23 rather than interleukin-12 is the critical cytokine for autoimmune inflammation of the brain
Cua, D. J., Sherlock, J., Chen, Y., Murphy, C. A., Joyce, B., Seymour, B., Lucian, L., To, W., Kwan, S., Churakova, T., et al. (2003) · Nature · doi:10.1038/nature01355 · Cited by 2,906
Novel p19 Protein Engages IL-12p40 to Form a Cytokine, IL-23, with Biological Activities Similar as Well as Distinct from IL-12
Oppmann, B., Lesley, R., Blom, B., Timans, J. C., Xu, Y., Hunte, B., Vega, F., Yu, N., Wang, J., Singh, K. P., et al. (2000) · Immunity · doi:10.1016/s1074-7613(00)00070-4 · Cited by 2,819
IL-21 initiates an alternative pathway to induce proinflammatory TH17 cells
Korn, T., Bettelli, E., Gao, W., Awasthi, A., Jäger, A., Strom, T. B., Oukka, M., & Kuchroo, V. K. (2007) · Nature · doi:10.1038/nature05970 · Cited by 1,896
Interleukin-23 Promotes a Distinct CD4 T Cell Activation State Characterized by the Production of Interleukin-17
Aggarwal, S., Ghilardi, N., Xie, M.-H., de Sauvage, F. J., & Gurney, A. L. (2003) · Journal of Biological Chemistry · doi:10.1074/jbc.m207577200 · Cited by 1,848

Flagged first, then by citations

Show all 44 references

Sorted by citations

Items 401–500 of 1,001

Adenosine A2A receptor modulates neuroimmune function through Th17/retinoid-related orphan receptor gamma t (RORγt) signaling in a BTBR T + Itpr3 tf /J mouse model of autism
Ansari, M. A., Nadeem, A., Attia, S. M., Bakheet, S. A., Raish, M., & Ahmad, S. F. (2017) · Cellular Signalling · doi:10.1016/j.cellsig.2017.04.014 · Cited by 59
Triple DMARD treatment in early rheumatoid arthritis modulates synovial T cell activation and plasmablast/plasma cell differentiation pathways
Walsh, A., Wechalekar, M., Guo, Y., Yin, X., Weedon, H., Proudman, S., Smith, M. D., & Nagpal, S. (2017) · PLoS ONE · doi:10.1371/journal.pone.0183928 · Cited by 56
Microglia promote autoimmune inflammation via the noncanonical NF-κB pathway
Jie, Z., Ko, C., Wang, H., Xie, X., Li, Y., Gu, M., Zhu, L., Yang, J., Gao, T., Ru, W., et al. (2021) · Science Advances · doi:10.1126/sciadv.abh0609 · Cited by 59
Chemokine-Driven Migration of Pro-Inflammatory CD4+ T Cells in CNS Autoimmune Disease
Heng, A. H. S., Han, C. W., Abbott, C. A., McColl, S. R., & Comerford, I. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.817473 · Cited by 61
“GM-CSF-deficient mice are highly resistant to EAE induction (38), and GM-CSFdeficient myelin-specific T cells are unable to transfer disease (35).”
Background
Astrocytic F as ligand expression is required to induce T ‐cell apoptosis and recovery from experimental autoimmune encephalomyelitis
Wang, X., Haroon, F., Karray, S., Deckert, M., & Schlüter, D. (2012) · European Journal of Immunology · doi:10.1002/eji.201242679 · Cited by 60
Highly polarized T h17 cells induce EAE via a T ‐bet independent mechanism
Grifka‐Walk, H. M., Lalor, S. J., & Segal, B. M. (2013) · European Journal of Immunology · doi:10.1002/eji.201343723 · Cited by 57
A two-amino-acid substitution in the transcription factor RORγt disrupts its function in TH17 differentiation but not in thymocyte development
He, Z., Ma, J., Wang, R., Zhang, J., Huang, Z., Wang, F., Sen, S., Rothenberg, E. V., & Sun, Z. (2017) · Nature Immunology · doi:10.1038/ni.3832 · Cited by 64
A distinct GM-CSF + T helper cell subset requires T-bet to adopt a T H 1 phenotype and promote neuroinflammation
Rasouli, J., Casella, G., Yoshimura, S., Zhang, W., Xiao, D., Garifallou, J., Gonzalez, M. V., Wiedeman, A., Kus, A., Mari, E. R., et al. (2020) · Science Immunology · doi:10.1126/sciimmunol.aba9953 · Cited by 57
“The relevant source of GM-CSF in EAE is TH cells, and both TH1 and TH17 cells need to be GM-CSF sufficient for their encephalitogenicity (8, 9).”
Background
OTUB1 inhibits CNS autoimmunity by preventing IFN‐γ‐induced hyperactivation of astrocytes
Wang, X., Mulas, F., Yi, W., Brunn, A., Nishanth, G., Just, S., Waisman, A., Brück, W., Deckert, M., & Schlüter, D. (2019) · The EMBO Journal · doi:10.15252/embj.2018100947 · Cited by 57
“…T helper (Th)1, interleukin (IL)-17-producing Th17, and granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing CD4 + T cells are shown to be key mediators of EAE, and all of them can induce EAE individually (Stromnes et al , 2008; Domingues et al , 2010; Codarri et al , 2011).”
Genetic and pharmacological inhibition of the nuclear receptor RORα regulates TH17 driven inflammatory disorders
Wang, R., Campbell, S., Amir, M., Mosure, S. A., Bassette, M. A., Eliason, A. D., Sundrud, M. S., Kamenecka, T. M., & Solt, L. A. (2021) · Nature Communications · doi:10.1038/s41467-020-20385-9 · Cited by 58
Protein Kinase C-θ Promotes Th17 Differentiation via Upregulation of Stat3
Kwon, M.-J., Ma, J., Ding, Y., Wang, R., & Sun, Z. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1102941 · Cited by 56
Effect of puberty on the immune system: Relevance to multiple sclerosis
Ucciferri, C. C., & Dunn, S. E. (2022) · Frontiers in Pediatrics · doi:10.3389/fped.2022.1059083 · Cited by 58
Small molecule inhibitors of RORγt for Th17 regulation in inflammatory and autoimmune diseases
Zeng, J., Li, M., Zhao, Q., Chen, M., Zhao, L., Wei, S., Yang, H., Zhao, Y., Wang, A., Shen, J., et al. (2023) · Journal of Pharmaceutical Analysis · doi:10.1016/j.jpha.2023.05.009 · Cited by 59
Meningeal mast cell-T cell crosstalk regulates T cell encephalitogenicity
Russi, A. E., Caulfield, M. E., Guo, Y. X., Lucchinetti, C. F., & Brown, M. A. (2016) · Journal of Autoimmunity · doi:10.1016/j.jaut.2016.06.015 · Cited by 55
IL‐1 signaling is critical for expansion but not generation of autoreactive GM‐CSF+ Th17 cells
Mufazalov, I. A., Schelmbauer, C., Regen, T., Kuschmann, J., Wanke, F., Gabriel, L. A., Hauptmann, J., Müller, W., Pinteaux, E., Kurschus, F. C., et al. (2016) · The EMBO Journal · doi:10.15252/embj.201694615 · Cited by 59
“Moreover, while the impact of IL-17 itself for EAE pathogenesis is still controversial (Haak et al , 2009; Ishigame et al , 2009), GM-CSF is indispensable for disease development (Codarri et al , 2011; El-Behi et al , 2011).”
Colony stimulating factors in the nervous system
Chiţu, V., Biundo, F., & Stanley, E. R. (2021) · Seminars in Immunology · doi:10.1016/j.smim.2021.101511 · Cited by 57
T Cell Intrinsic Function of the Noncanonical NF-κB Pathway in the Regulation of GM-CSF Expression and EAE Pathogenesis
Yu, J., Zhou, X.-F., Nakaya, M., Jin, W., Cheng, X.-H., & Sun, S.-C. (2014) · Journal of Immunology · doi:10.4049/jimmunol.1303237 · Cited by 54
Satb1 regulates the effector program of encephalitogenic tissue Th17 cells in chronic inflammation
Yasuda, K., Kitagawa, Y., Kawakami, R., Isaka, Y., Watanabe, H., Kondoh, G., Kohwi-shigematsu, T., Sakaguchi, S., & Hirota, K. (2019) · Nature Communications · doi:10.1038/s41467-019-08404-w · Cited by 55
Noncanonical STAT3 activity sustains pathogenic Th17 proliferation and cytokine response to antigen
Poholek, C. H., Raphael, I., Wu, D., Revu, S. K., Rittenhouse, N., Uche, U. N., Majumder, S., Kane, L., Poholek, A. C., & McGeachy, M. J. (2020) · The Journal of Experimental Medicine · doi:10.1084/jem.20191761 · Cited by 57
“In contrast, STAT3 deletion after IL-17 production did not affect PMA- and ionomycin-elicited cytokine production or expression of other previously identified IL-23–dependent effector molecules (Codarri et al., 2011; Du et al., 2016; El-Behi et al., 2011; Hirota et al., 2011; Jain et al., 2016; McGeachy et al., 2009).”
Background
Aging weakens Th17 cell pathogenicity and ameliorates experimental autoimmune uveitis in mice
Li, H., Zhu, L., Wang, R., Xie, L., Ren, J., Ma, S., Zhang, W., Liu, X., Huang, Z., Chen, B., et al. (2021) · Protein & Cell · doi:10.1007/s13238-021-00882-3 · Cited by 53
“Expression of GM-CSF is a mark of pathogenic Th17 cells (Codarri et al., 2011; El-Behi et al., 2011b).”
Background
Chemokine-mediated redirection of T cells constitutes a critical mechanism of glucocorticoid therapy in autoimmune CNS responses
Schweingruber, N., Fischer, H. J., Fischer, L., van den Brandt, J., Karabinskaya, A., Labi, V., Villunger, A., Kretzschmar, B., Huppke, P., Simons, M., et al. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1248-4 · Cited by 54
“However, neither IFNγ nor Il-17 alone is essential for the pathogenic potential of effector T cells [12, 16] but rather gM-CSF seems to be a crucial factor in eAe [6, 11, 24].”
Background
Myelin Basic Protein-Specific TCR/HLA-DRB5*01:01 Transgenic Mice Support the Etiologic Role of DRB5*01:01 in Multiple Sclerosis
Quandt, J. A., Huh, J., Baig, M. S., Yao, K., Ito, N., Bryant, M., Kawamura, K., Pinilla, C., McFarland, H. F., Martinꝉ, R., et al. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1103087 · Cited by 55
“In addition, development of GM-CSF–producing Th1/Th17 cells, which play an essential role in the development of EAE (62, 63), was increased in TL3A6/ DR2a Tg mice (Fig.”
Background
Evaluation of the effect of GM-CSF blocking on the phenotype and function of human monocytes
Lotfi, N., Zhang, G., Esmaeil, N., & Rostami, A. M. (2020) · Scientific Reports · doi:10.1038/s41598-020-58131-2 · Cited by 52
IL-21 Is a Central Memory T Cell–Associated Cytokine That Inhibits the Generation of Pathogenic Th1/17 Effector Cells
Kastirr, I., Maglie, S., Paroni, M., Alfen, J. S., Nizzoli, G., Sugliano, E., Crosti, M., Moro, M., Steckel, B., Steinfelder, S., et al. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1400775 · Cited by 57
“Moreover, the production of the cytokine GM-CSF by Th17 cells is important for their pathogenic function (12, 16, 17).”
Background
Reduction in lipophilicity improved the solubility, plasma–protein binding, and permeability of tertiary sulfonamide RORc inverse agonists
Fauber, B. P., René, O., Boenig, G. D. L., Burton, B., Deng, Y., Eidenschenk, C., Everett, C., Gobbi, A., Hymowitz, S. G., Johnson, A. R., et al. (2014) · Bioorganic & Medicinal Chemistry Letters · doi:10.1016/j.bmcl.2014.06.048 · Cited by 53
The role of IL-12/23 in T cell–related chronic inflammation: implications of immunodeficiency and therapeutic blockade
Schurich, A., Raine, C., Morris, V., & Ciurtin, C. (2017) · Rheumatology · doi:10.1093/rheumatology/kex186 · Cited by 53
Neural precursor cell–secreted TGF-β2 redirects inflammatory monocyte-derived cells in CNS autoimmunity
Feo, D. D., Merlini, A., Brambilla, E., Ottoboni, L., Laterza, C., Menon, R., Srinivasan, S., Farina, C., Manteiga, J. M. G., Butti, E., et al. (2017) · Journal of Clinical Investigation · doi:10.1172/jci92387 · Cited by 54
PSGL‐1 and E/P‐selectins are essential for T‐cell rolling in inflamed CNS microvessels but dispensable for initiation of EAE
Sathiyanadan, K., Coisne, C., Enzmann, G., Deutsch, U., & Engelhardt, B. (2014) · European Journal of Immunology · doi:10.1002/eji.201344214 · Cited by 51
Selective IL-27 production by intestinal regulatory T cells permits gut-specific regulation of TH17 cell immunity
Lin, C., Wu, C.-J., Cho, S., Patkar, R., Huth, W. J., Lin, L.-L., Chen, M., Israelsson, E., Betts, J., Niedzielska, M., et al. (2023) · Nature Immunology · doi:10.1038/s41590-023-01667-y · Cited by 55
Re-establishing immune tolerance in multiple sclerosis: focusing on novel mechanisms of mesenchymal stem cell regulation of Th17/Treg balance
Hu, H., Li, H., Li, R., Liu, P., & Liu, H. (2024) · Journal of Translational Medicine · doi:10.1186/s12967-024-05450-x · Cited by 56
Targeting cytokine networks in neuroinflammatory diseases
Becher, B., Derfuss, T. J., & Liblau, R. (2024) · Nature Reviews Drug Discovery · doi:10.1038/s41573-024-01026-y · Cited by 56
“This puzzling observation was later explained when IL-23 was shown to induce secretion of the cytokine GM-CSF in T H 17 cells 88 , which led to a severe CNS pathology in the animal model 89 .”
NOD-like receptors and RIG-I-like receptors in human eosinophils: activation by NOD1 and NOD2 agonists
Kvarnhammar, A. M., Petterson, T., & Cardell, L. (2011) · Immunology · doi:10.1111/j.1365-2567.2011.03492.x · Cited by 52
IL ‐17 A activates ERK 1/2 and enhances differentiation of oligodendrocyte progenitor cells
Rodgers, J. M., Robinson, A. P., Rosler, E. S., Lariosa-Willingham, K. D., Persons, R. E., Dugas, J. C., & Miller, S. D. (2014) · Glia · doi:10.1002/glia.22783 · Cited by 53
“Using the mouse model of MS, experimental autoimmune encephalomyelitis (EAE), a large body of work has investigated Th17 cells and whether their production of IL17A is essential to driving immunopathology and disease progression (Codarri et al., 2011; Jager et al., 2009).”
Method
Gatekeeper role of brain antigen‐presenting CD11c+ cells in neuroinflammation
Paterka, M., Siffrin, V., Voß, J. O., Werr, J., Hoppmann, N., Gollan, R., Belikan, P., Bruttger, J., Birkenstock, J., Jung, S., et al. (2015) · The EMBO Journal · doi:10.15252/embj.201591488 · Cited by 52
“In addition, also GM-CSF deficient Th1 cells exhibited less encephalitogenicity (Codarri et al , 2011).”
Influential
Comparative effect of 25(OH)D3 and 1,25(OH)2D3 on Th17 cell differentiation
Fawaz, L. M., Mrad, M. F., Kazan, J. M., Sayegh, S., Akika, R., & Khoury, S. J. (2016) · Clinical Immunology · doi:10.1016/j.clim.2016.02.011 · Cited by 52
Dysregulation of proinflammatory versus anti-inflammatory human TH17 cell functionalities in the autoinflammatory Schnitzler syndrome
Noster, R., de Koning, H. D., Maier, E., Prelog, M., Lainka, E., & Zielinski, C. E. (2016) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2015.12.1338 · Cited by 53
“Recently, GM-CSF, but not IL-17, has been shown to be the crucial pathogenic TH17 cell cytokine in the EAE mouse model for multiple sclerosis and to be also associated with human multiple sclerosis.(12,14) This demonstrates that the pathogenicity of TH17 cells is determined by specific cytokine coexpression patterns r…”
Background
Postarrest stalling rather than crawling favors CD8 + over CD4 + T‐cell migration across the blood–brain barrier under flow in vitro
Rudolph, H., Klopstein, A., Gruber, I., Blatti, C., Lyck, R., & Engelhardt, B. (2016) · European Journal of Immunology · doi:10.1002/eji.201546251 · Cited by 54
Extracellular Purine Metabolism Is the Switchboard of Immunosuppressive Macrophages and a Novel Target to Treat Diseases With Macrophage Imbalances
Ohradanova‐Repic, A., Machacek, C., Charvet, C., Lager, F., Roux, D. L., Platzer, R., Leksa, V., Mitulović, G., Burkard, T. R., Zlabinger, G. J., et al. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00852 · Cited by 53
“In mice, GM-CSF expression is directly confined to the Th17 subset (72, 73).”
Background
Deficiency of Socs3 leads to brain-targeted experimental autoimmune encephalomyelitis via enhanced neutrophil activation and ROS production
Yan, Z., Yang, W., Parkitny, L., Gibson, S. A., Lee, K. S., Collins, F., Deshane, J. S., Cheng, W., Weinmann, A. S., Wei, H., et al. (2019) · JCI Insight · doi:10.1172/jci.insight.126520 · Cited by 59
Tissue-restricted control of established central nervous system autoimmunity by TNF receptor 2–expressing Treg cells
Ronin, É., Pouchy, C., Khosravi, M., Hilaire, M., Grégoire, S., Casrouge, A., Kassem, S., Sleurs, D., Martin, G. H., Chanson, N., et al. (2021) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2014043118 · Cited by 62
“GM-CSF, which is the major pathogenic cytokine produced by Tconv cells in EAE (27), was significantly increased in icKO mice compared with control mice after both anti-CD3 and immunizing myelin antigen stimulation (Fig.”
Background
IL-7/IL-7 Receptor Signaling Differentially Affects Effector CD4+ T Cell Subsets Involved in Experimental Autoimmune Encephalomyelitis
Arbelaez, C. A., Glatigny, S., Duhen, R., Eberl, G., Oukka, M., & Bettelli, E. (2015) · The Journal of Immunology · doi:10.4049/jimmunol.1403135 · Cited by 51
“Furthermore, consistent with the idea that IL-7 modulates the differentiation of effector T cells, we found that in all Th-polarizing conditions tested, IL-7 promotes GM-CSF production, a cytokine that has been implicated in the pathogenicity of T cells during EAE (9, 10).”
Pathogenesis of the immune reconstitution inflammatory syndrome in HIV-infected patients
Martin‐Blondel, G., Mars, L. T., & Liblau, R. (2012) · Current Opinion in Infectious Diseases · doi:10.1097/qco.0b013e328352b664 · Cited by 52
IL-22 Mediates Host Defense against an Intestinal Intracellular Parasite in the Absence of IFN-γ at the Cost of Th17-Driven Immunopathology
Stange, J., Hepworth, M. R., Rausch, S., Zajic, L. B., Kühl, A. A., Uyttenhove, C., Renauld, J., Hartmann, S., & Lucius, R. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1102062 · Cited by 51
Diverting T helper cell trafficking through increased plasticity attenuates autoimmune encephalomyelitis
Califano, D., Sweeney, K. J., Le, H., VanValkenburgh, J., Yager, E. J., O’Connor, W., Kennedy, J. S., Jones, D. M., & Avram, D. (2013) · Journal of Clinical Investigation · doi:10.1172/jci70103 · Cited by 51
“GM-CSF was recently demonstrated to be a critical cytokine for EAE pathology (5, 6); however, GM-CSF has multiple roles in the immune system, such as stimulating, together with IL-4, dendritic cell maturation and induction of RA production (37).”
Small molecule mediated inhibition of ROR γ ‐dependent gene expression and autoimmune disease pathology in vivo
Banerjee, D., Zhao, L., Wu, L., Palanichamy, A., Ergün, A., Peng, L., Quigley, C., Hamann, S., Dunstan, R. W., Cullen, P. F., et al. (2015) · Immunology · doi:10.1111/imm.12570 · Cited by 50
Interleukin‐17‐ and interleukin‐22‐secreting myelin‐specific CD 4+ T cells resistant to corticoids are related with active brain lesions in multiple sclerosis patients
Wing, A. C., Hygino, J., Ferreira, T. B., Kasahara, T. M., Barros, P. O., Sacramento, P. M., de Andrade, R. M., Camargo, S. M. D. G. G., Rueda, F., Alves‐Leon, S. V., et al. (2015) · Immunology · doi:10.1111/imm.12552 · Cited by 51
IL-3 promotes the development of experimental autoimmune encephalitis.
Renner, K., Hellerbrand, S., Hermann, F., Riedhammer, C., Talke, Y., Schiechl, G., Gomez, M., Kutzi, S., Halbritter, D., Goebel, N., et al. (2016) · JCI Insight · doi:10.1172/jci.insight.87157 · Cited by 53
“Acknowledgments This work was supported by grants from the Deutsche Forschungsgemeinschaft to HB and MM (21-98) and Regensburg Center for Interventional Immunology (RCI) to RW, HB, and MM.”
Neutrophil perversion in demyelinating autoimmune diseases: Mechanisms to medicine
Casserly, C. S., Nantes, J. C., Hawkins, R. W., & Vallières, L. (2017) · Autoimmunity Reviews · doi:10.1016/j.autrev.2017.01.013 · Cited by 52
Targeting the GM-CSF receptor for the treatment of CNS autoimmunity
Ifergan, I., Davidson, T. S., Kébir, H., Xu, D., Palacios-Macapagal, D., Cann, J. A., Rodgers, J. M., Hunter, Z. N., Pittet, C. L., Beddow, S. A., et al. (2017) · Journal of Autoimmunity · doi:10.1016/j.jaut.2017.06.005 · Cited by 55
“Furthermore, since GM-CSF is able to act as a chemotactic agent [17,44,45], and was found to be involved in recruiting myeloid cells into the CNS critical for EAE development [3], it is highly likely that in addition to reduce myeloid cell activation, anti-GM-CSF Rα reduced cell migratory capacity to the CNS, leading…”
Background
Foxp3-independent mechanism by which TGF-β controls peripheral T cell tolerance
Oh, S. A., Liu, M., Nixon, B. G., Kang, D., Toure, A., Bivona, M. R., & Li, M. O. (2017) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1706356114 · Cited by 52
“Whereas inflammatory monocytes are wellknown innate immune cells mobilized during infection for host defense responses (35), recent studies have revealed that inflammatory monocytes are also essential for the induction of tissue damage in immunization models of autoimmune diseases such as experimental autoimmune encep…”
BackgroundInfluential
Mast Cells and Innate Lymphoid Cells: Underappreciated Players in CNS Autoimmune Demyelinating Disease
Brown, M. A., & Weinberg, R. B. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00514 · Cited by 52
The Multifaceted Role of Th17 Lymphocytes and Their Associated Cytokines in Cancer
Alizadeh, D., Katsanis, E., & Larmonier, N. (2013) · Clinical and Developmental Immunology · doi:10.1155/2013/957878 · Cited by 55
“We provide an overview on the requirements for Th17 development and the direct or indirect impact of Th17 lymphocytes and the cytokines they produce on antitumor responses.”
Pathogenic Bhlhe40+ GM-CSF+ CD4+ T cells promote indirect alloantigen presentation in the GI tract during GVHD
Piper, C., Zhou, V., KOMOROWSKI, R. A., Szabó, A., Vincent, B. G., Serody, J. S., Alegre, M., Edelson, B. T., Taneja, R., & Drobyski, W. R. (2019) · Blood · doi:10.1182/blood.2019001696 · Cited by 49
Complementary action of granulocyte macrophage colony-stimulating factor and interleukin-17A induces interleukin-23, receptor activator of nuclear factor-κB ligand, and matrix metalloproteinases and drives bone and cartilage pathology in experimental arthritis: rationale for combination therapy in rheumatoid arthritis
van Nieuwenhuijze, A. E. M., van de Loo, F. A. J., Walgreen, B., Bennink, M. B., Helsen, M. M. A., van den Bersselaar, L., Wicks, I. P., van den Berg, W. B., & Koenders, M. I. (2015) · Arthritis Research & Therapy · doi:10.1186/s13075-015-0683-5 · Cited by 50
“GM-CSF has recently been identified as a key player in Th17-mediated inflammation [16, 17, 23, 24].”
BackgroundInfluential
Involvement of the IL-1 system in experimental autoimmune encephalomyelitis and multiple sclerosis: Breaking the vicious cycle between IL-1β and GM-CSF
Paré, A., Mailhot, B., Lévesque, S. A., & Lacroix, S. (2016) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2016.07.146 · Cited by 51
18β-glycyrrhetinic acid suppresses experimental autoimmune encephalomyelitis through inhibition of microglia activation and promotion of remyelination
Zhou, J., Cai, W., Jin, M., Xu, J., Wang, Y., Xiao, Y., Li, H., Wang, B., Zhang, Y., Han, J., et al. (2015) · Scientific Reports · doi:10.1038/srep13713 · Cited by 50
Islet Antigen-Specific Th17 Cells Can Induce TNF-α–Dependent Autoimmune Diabetes
Li, C.-R., Mueller, E. E., & Bradley, L. M. (2014) · The Journal of Immunology · doi:10.4049/jimmunol.1301742 · Cited by 48
“Abbreviations used in this article: EAE, experimental autoimmune encephalomyelitis; LN, lymph node; PLN, pancreatic lymph node; T1D, type 1 diabetes; WT, wildtype.”
ResultInfluential
Low-Voltage-Activated Ca V 3.1 Calcium Channels Shape T Helper Cell Cytokine Profiles
Wang, H., Zhang, X., Xue, L., Xing, J., Jouvin, M.-H., Putney, J. W., Anderson, M. P., Trebak, M., & Kinet, J.-P. (2016) · Immunity · doi:10.1016/j.immuni.2016.01.015 · Cited by 51
“Because granulocyte-macrophage colony stimulating factor (GM-CSF) has proven to be a critical factor in the encephalitogenicity of both Th1 and Th17 cells in EAE model (Codarri et al., 2011; El-Behi et al., 2011), we analyzed the infiltrating cells in the central nervous system (CNS).”
BackgroundInfluential
High levels of circulating GM-CSF+CD4+ T cells are predictive of poor outcomes in sepsis patients: a prospective cohort study
Huang, H., Wang, S.-Y., Jiang, T., Fan, R., Zhang, Z., Mu, J., Li, K., Wang, Y., Jin, L., Lin, F., et al. (2018) · Cellular & Molecular Immunology · doi:10.1038/s41423-018-0164-2 · Cited by 47
Targeting Granulocyte-Monocyte Colony-Stimulating Factor Signaling in Rheumatoid Arthritis: Future Prospects
Crotti, C., Agape, E., Becciolini, A., Biggioggero, M., & Favalli, E. G. (2019) · Drugs · doi:10.1007/s40265-019-01192-z · Cited by 49
Dulaglutide Modulates the Development of Tissue-Infiltrating Th1/Th17 Cells and the Pathogenicity of Encephalitogenic Th1 Cells in the Central Nervous System
Chiou, H.-Y. C., Lin, M., Hsiao, P., Chen, C., Chiao, S., Lin, T.-Y., Chen, Y., Wu, D.-C., & Lin, M. (2019) · International Journal of Molecular Sciences · doi:10.3390/ijms20071584 · Cited by 52
microRNA-92a promotes CNS autoimmunity by modulating the regulatory and inflammatory T cell balance
Fujiwara, M., Raheja, R., Garo, L. P., Ajay, A. K., Kadowaki-Saga, R., Karandikar, S. H., Gabriely, G., Krishnan, R., Beynon, V., Paul, A., et al. (2022) · Journal of Clinical Investigation · doi:10.1172/jci155693 · Cited by 50
“Furthermore, Foxo1 has been shown to inhibit this RORγt-mediated transactivation of Il1r1 and Il23r (26, 43, 46) by preventing RORγt from binding to the Il1r1 and Il23r promoters (21, 22).”
BackgroundInfluential
Central Nervous System Macrophages in Health and Disease
Hove, H. V., Feo, D. D., Greter, M., & Becher, B. (2025) · Annual Review of Immunology · doi:10.1146/annurev-immunol-082423-041334 · Cited by 53
Roles of T helper 17 cells and interleukin‐17 in neuroautoimmune diseases with emphasis on multiple sclerosis and Guillain‐Barré syndrome as well as their animal models
Wang, X., Ma, C., Wu, J., & Zhu, J. (2013) · Journal of Neuroscience Research · doi:10.1002/jnr.23233 · Cited by 49
“…the lack of GM-CSF rendered complete resistance to EAE, whereas the expression of GM-CSF in IL-17- and IFN-g-deficient T cells still effectively initiated neuroinflammation in EAE, which strongly supports a nonredundant effect of GMCSF in driving autoimmune inflammation (Codarri et al., 2011).”
Background
Exacerbation of experimental autoimmune encephalomyelitis in mice deficient for DCIR, an inhibitory C-type lectin receptor
Seno, A., Maruhashi, T., Kaifu, T., Yabe, R., Fujikado, N., Ma, G., Ikarashi, T., Kakuta, S., & Iwakura, Y. (2014) · EXPERIMENTAL ANIMALS · doi:10.1538/expanim.14-0079 · Cited by 51
“The secreted iL-23 in turn promotes Th17 cell differentiation, forming an amplification loop [5, 9].”
Background
Treatment with MOG-DNA vaccines induces CD4+CD25+FoxP3+ regulatory T cells and up-regulates genes with neuroprotective functions in experimental autoimmune encephalomyelitis
Fissolo, N., Costa, C., Nurtdinov, R., Bustamante, M. F., Llombart, V., Mansilla, M. J., Espejo, C., Montalbán, X., & Comabella, M. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-139 · Cited by 48
Cutting Edge: Suppression of GM-CSF Expression in Murine and Human T Cells by IL-27
Young, A., Linehan, E., Hams, E., Hall, A. O., McClurg, A. E., Johnston, J. A., Hunter, C. A., Fallon, P. G., & Fitzgerald, D. C. (2012) · The Journal of Immunology · doi:10.4049/jimmunol.1200131 · Cited by 49
“As IFN-γ can inhibit GM-CSF expression (7) and is induced by IL-27 (22), we examined if IFN-γ mediated suppression of GM-CSF by IL-27.”
Influential
Cutting Edge: MicroRNA-223 Regulates Myeloid Dendritic Cell–Driven Th17 Responses in Experimental Autoimmune Encephalomyelitis
Ifergan, I., Chen, S., Zhang, B., & Miller, S. D. (2016) · The Journal of Immunology · doi:10.4049/jimmunol.1501965 · Cited by 48
“In contrast, KO APCs were significantly less capable of inducing differentiation of IL-17–producing and GM-CSF– producing Th17 cells, with virtually no GM-CSF, a cytokine reported to be essential in the pathogenic process of EAE (26), produced at day 5.”
Background
Inflammatory Th17 Cells Express Integrin αvβ3 for Pathogenic Function
Du, F., Garg, A. V., Kosar, K., Majumder, S., Kugler, D. G., Hernández-Mir, G., Maggio, M. J., Henkel, M., Lacy‐Hulbert, A., & McGeachy, M. J. (2016) · Cell Reports · doi:10.1016/j.celrep.2016.06.065 · Cited by 49
“IL-23 is also required for granulocyte-monocyte colony stimulating factor (GM-CSF) production by Th17 cells, which is critical for EAE induction (Codarri et al., 2011; El-Behi et al., 2011).”
Background
GM-CSF is not essential for experimental autoimmune encephalomyelitis but promotes brain-targeted disease.
Pierson, E., & Goverman, J. (2017) · JCI Insight · doi:10.1172/jci.insight.92362 · Cited by 51
Protein Kinase CK2 Controls the Fate between Th17 Cell and Regulatory T Cell Differentiation
Gibson, S. A., Yang, W., Yan, Z., Liu, Y., Rowse, A. L., Weinmann, A. S., Qin, H., & Benveniste, E. N. (2017) · The Journal of Immunology · doi:10.4049/jimmunol.1601912 · Cited by 47
“Furthermore, Th17 cell–derived GM-CSF is critical for disease progression (45, 46).”
Background
Exploring Non-Metabolic Functions of Glycolytic Enzymes in Immunity
Seki, S. M., & Gaultier, A. (2017) · Frontiers in Immunology · doi:10.3389/fimmu.2017.01549 · Cited by 49
“In a manner reminiscent of direct repression of IFN-γ and IL-2 mRNA translation by the glycolytic enzyme GAPDH (31, 32), LDH-A has been reported to bind to 3′AU-rich elements in GM-CSF mRNA (84).”
Background
Role of the β Common (βc) Family of Cytokines in Health and DiseasePreprint
Hercus, T. R., Kan, W. L., Broughton, S. E., Tvorogov, D., Ramshaw, H. S., Sandow, J. J., Nero, T. L., Dhagat, U., Thompson, E. J., Shing, K. S. C. T., et al. (2017) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a028514 · Cited by 51
Selective visuoconstructional impairment following mild COVID-19 with inflammatory and neuroimaging correlation findings
de Paula, J. J., de Paiva, R. E. R. P., Silva, N. G. S. E., Rosa, D. V., Duran, F., Coimbra, R. S., Costa, D. D. S., Dutenhefner, P. R., Oliveira, H. S. D., Camargos, S., et al. (2022) · Molecular Psychiatry · doi:10.1038/s41380-022-01632-5 · Cited by 51
“CSF is essential for the pathogenesis of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, mediated by encephalitogenic T helper cells that produce IL-17 (Th17 cells) [64].”
Background
Zinc aspartate suppresses T cell activation in vitro and relapsing experimental autoimmune encephalomyelitis in SJL/J mice
Stoye, D., Schubert, C., Goihl, A., Guttek, K., Reinhold, A., Brocke, S., Grüngreiff, K., & Reinhold, D. (2012) · BioMetals · doi:10.1007/s10534-012-9532-z · Cited by 47
“While IL–17 was shown to play an important role in the development of EAE (Hofstetter et al. 2007; Komiyama et al. 2006), other reports have challenged these findings (Haak et al. 2009; Codarri et al. 2011).”
BackgroundResult
CD28/CTLA‐4/B7 costimulatory pathway blockade affects regulatory T‐cell function in autoimmunity
Vogel, I., Kasran, A., Cremer, J., Kim, Y., Boon, L., Gool, S. W. V., & Ceuppens, J. L. (2015) · European Journal of Immunology · doi:10.1002/eji.201445190 · Cited by 47
The role of iron metabolism in the pathogenesis and treatment of multiple sclerosis
Duarte-Silva, E., Meuth, S. G., & Peixoto, C. A. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1137635 · Cited by 46
GM-CSF Modulates Autoantibody Production and Skin Blistering in Experimental Epidermolysis Bullosa Acquisita
Samavedam, U. K. S. R. L., Iwata, H., Müller, S., Schulze, F. S., Recke, A., Schmidt, E., Zillikens, D., & Ludwig, R. J. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1301556 · Cited by 46
“inflammation in models of arthritis (10–13), experimental autoimmune encephalitis (14), psoriasis (15), and nephritis (16).”
Background
Interleukin-36γ is expressed by neutrophils and can activate microglia, but has no role in experimental autoimmune encephalomyelitis
Bozoyan, L., Dumas, A., Patenaude, A., & Vallières, L. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0392-7 · Cited by 46
“For example: GM-CSF derives from T cells and promotes dendritic cell recruitment [20, 21],”
Background
Toso controls encephalitogenic immune responses by dendritic cells and regulatory T cells
Brenner, D., Brüstle, A., Lin, G. H. Y., Lang, P. A., Duncan, G. S., Knobbe-Thomsen, C. B., Paul, M. S., Reardon, C., Tusche, M. W., Snow, B. E., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1323166111 · Cited by 46
“Several groups have reported that functional Th17 cells are important for the recruitment of inflammatory macrophages to the CNS that sustain neuroinflammation (25, 29, 30).”
Background
Targeting the B7 Family of Co-Stimulatory Molecules
Podojil, J. R., & Miller, S. D. (2012) · BioDrugs · doi:10.1007/s40259-012-0001-6 · Cited by 48
“In contrast, the more critical cytokine in the induction of EAE disease may be GM-CSF, since in the absence of GM-CSF expression EAE disease induction is eliminated [43].”
Endogenous, or therapeutically induced, type I interferon responses differentially modulate Th1/Th17‐mediated autoimmunity in the CNS
Kalinke, U., & Prinz, M. (2012) · Immunology and Cell Biology · doi:10.1038/icb.2012.8 · Cited by 45
Mechanistic Sharing Between NK Cells in ABMR and Effector T Cells in TCMR
Parkes, M. D., Halloran, P., & Hidalgo, L. (2018) · American Journal of Transplantation · doi:10.1111/ajt.14410 · Cited by 46
“IFNG produced by activated T and NK cells increases antigen availability in rejection by enhancing HLA expression on endothelial cells and antigen presenting cells (39,40) in addition to its multiple synergies with TNF (41–43) and CSF2 (44) CSF2 is often considered a key TH17 effector cytokine (45,46), yet our data sh…”
Background
Dopaminergic Stimulation of Myeloid Antigen-Presenting Cells Attenuates Signal Transducer and Activator of Transcription 3-Activation Favouring the Development of Experimental Autoimmune Encephalomyelitis
Prado, C. E., Gaiazzi, M., González, H., Ugalde, V., Figueroa, A., Osorio‐Barrios, F., López, E., Lladser, Á., Rasini, E., Marino, F., et al. (2018) · Frontiers in Immunology · doi:10.3389/fimmu.2018.00571 · Cited by 44
“Thus, the pro-inflammatory cytokines IL-17, IFN-γ, and GM-CSF produced by CD4+ T-cells contribute to the development of EAE, although the latter plays a major role (14, 16).”
BackgroundMethodInfluential
Cytokines and Chemokines in the Pathogenesis of Experimental Autoimmune Encephalomyelitis
Karpus, W. J. (2020) · The Journal of Immunology · doi:10.4049/jimmunol.1900914 · Cited by 48
Role of the Immunogenic and Tolerogenic Subsets of Dendritic Cells in Multiple Sclerosis
Xie, Z., Zhang, H., Wu, X., Zhu, J., Ma, D., & Jin, T. (2015) · Mediators of Inflammation · doi:10.1155/2015/513295 · Cited by 46
Innate and adaptive immune abnormalities underlying autoimmune diseases: the genetic connections
Chi, X., Huang, M., Tu, H., Zhang, B., Lin, X., Xu, H., Dong, C., & Hu, X. (2023) · Science China Life Sciences · doi:10.1007/s11427-021-2187-3 · Cited by 47
“Cytotoxic Trm cells expressing IFN-γ or IL-17A have been identified in vitiligo and psoriasis patients.”
BackgroundInfluential
ITE, A Novel Endogenous Nontoxic Aryl Hydrocarbon Receptor Ligand, Efficiently Suppresses EAU and T-Cell–Mediated Immunity
Nugent, L. F., Shi, G., Vistica, B. P., Ogbeifun, O., Hinshaw, S. J. H., & Gery, I. (2013) · Investigative Ophthalmology & Visual Science · doi:10.1167/iovs.12-11479 · Cited by 45
“In addition to the mentioned three cytokines, we also measured the levels of GM-CSF, a cytokine that was recently reported to play a major role in the immunopathogenic process of EAE.23,24 As shown in Figures 4A and 4B, LN cells from ITE-treated mice secreted lower levels of GM-CSF than did their controls.”
Background
Decreased RORC-dependent silencing of prostaglandin receptor EP2 induces autoimmune Th17 cells
Kofler, D. M., Marson, A., Dominguez‐Villar, M., Xiao, S., Kuchroo, V. K., & Hafler, D. A. (2014) · Journal of Clinical Investigation · doi:10.1172/jci72973 · Cited by 44
“GM-CSF production in helper T cells is driven by RORγt (39), and the encephalitogenicity of Th17 cells in EAE is dependent on their production of GM-CSF (40).”
IL-23 Promotes Myocardial I/R Injury by Increasing the Inflammatory Responses and Oxidative Stress Reactions
Hu, X., Ma, R., Lu, J., Zhang, K., Xu, W., Jiang, H., & Da, Y. (2016) · Cellular Physiology and Biochemistry · doi:10.1159/000445572 · Cited by 45
CCAAT/Enhancer-binding protein β promotes pathogenesis of EAE
Simpson-Abelson, M. R., Hernández-Mir, G., Childs, E. E., Cruz, J. A., Poholek, A. C., Chattopadhyay, A., Gaffen, S. L., & McGeachy, M. J. (2017) · Cytokine · doi:10.1016/j.cyto.2017.01.005 · Cited by 44
SerpinB1 controls encephalitogenic T helper cells in neuroinflammation
Hou, L., Rao, D. A., Yuki, K., Cooley, J., Henderson, L. A., Jonsson, A. H., Kaiserman, D., Gorman, M., Nigrovic, P. A., Bird, P. I., et al. (2019) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1905762116 · Cited by 43
TH Cells and Cytokines in Encephalitogenic Disorders
Krishnarajah, S., & Becher, B. (2022) · Frontiers in Immunology · doi:10.3389/fimmu.2022.822919 · Cited by 49
RORγt agonist enhances anti-PD-1 therapy by promoting monocyte-derived dendritic cells through CXCL10 in cancers
Xia, L., Tian, E., Yu, M., Liu, C., Shen, L., Huang, Y., Wu, Z., Tian, J., Yu, K., Wang, Y., et al. (2022) · Journal of Experimental & Clinical Cancer Research · doi:10.1186/s13046-022-02289-2 · Cited by 44
Molecular underpinnings of Th17 immune-regulation and their implications in autoimmune diabetes
Kumar, P., & Subramaniyam, G. (2014) · Cytokine · doi:10.1016/j.cyto.2014.10.010 · Cited by 46
“It is evident that blockade of GM-CSF signaling protected mice from autoimmunity [93].”
Background
RORγt-specific transcriptional interactomic inhibition suppresses autoimmunity associated with T H 17 cells
Park, T. Y., Park, S.-D., Cho, J.-Y., Moon, J., Kim, N.-Y., Park, K., Seong, R. H., Lee, S., Morio, T., Bothwell, A. L. M., et al. (2014) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1413687112 · Cited by 45
T ‐bet is essential for T h1‐mediated, but not T h17‐mediated, CNS autoimmune disease
O’Connor, R. A., Cambrook, H., Huettner, K., & Anderton, S. M. (2013) · European Journal of Immunology · doi:10.1002/eji.201343689 · Cited by 44
Cytokine amplification and macrophage effector functions in aortic inflammation and abdominal aortic aneurysm formation.
Ijaz, T., Tilton, R., & Brasier, A. (2016) · Journal of Thoracic Disease · doi:10.21037/jtd.2016.06.37 · Cited by 43
“GM-CSF is a chemotactic cytokine involved in macrophage maturation that is secreted locally by aortic fibroblasts (26), and infiltrating monocyte/macrophages and Th17 cells (27).”
Background
Physical plasma and leukocytes – immune or reactive?
Bekeschus, S., Seebauer, C., Wende, K., & Schmidt, A. (2018) · Biological Chemistry · doi:10.1515/hsz-2018-0224 · Cited by 45
“, 2009), and granulocyte-macrophage colony-stimulating factor that drives autoinflamation (Codarri et al., 2011).”
Background
Upregulated tissue expression of T helper (Th) 17 pathogenic interleukin (IL)-23 and IL-1β in Hashimoto’s thyroiditis but not in Graves’ disease
Zaķe, T., Skuja, S., Kalere, I., Konrāde, I., & Groma, V. (2019) · Endocrine Journal · doi:10.1507/endocrj.ej18-0396 · Cited by 46

Authors: Codarri, L., Gyülvészi, G., Tosevski, V., Hesske, L., Fontana, A., Magnenat, L., Suter, T., & Becher, B.
Affiliations: University Hospital Zurich (CH)
University of Zurich (CH)
Merck Serono S.A. (Switzerland) (CH)
Corresponding author: Becher, Burkhard
ORCID: Magnenat, Laurent
Suter, Tobias
Becher, Burkhard
Venue: Nature Immunology
Publisher: Springer Science and Business Media LLC
Published: 2011-04-24
Volume: 12
Issue: 6
Pages: 560-567
ISSN: 1529-2908 (ISSN-L)
1529-2916
DOI: 10.1038/ni.2027
OpenAlex: W2157837362
Cited by: 1,191
References: 44
Citations by year: 2026: 31 · 2025: 48 · 2024: 60 · 2023: 53 · 2022: 61 · 2021: 73 · 2020: 85 · 2019: 83 · 2018: 72 · 2017: 99 · 2016: 96 · 2015: 117 · 2014: 103 · 2013: 98 · 2012: 82
FWCI: 70.23
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Nature Immunology (publishedVersion)
PubMed (publishedVersion)
Zurich Open Repository and Archive (University of Zurich) (submittedVersion)
Topics: Health Sciences › Medicine › Clinical Neurology › Multiple Sclerosis Research Studies
Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords: RORγt, GM-CSF, experimental autoimmune encephalomyelitis, T helper cells, IL-23, autoimmune neuroinflammation, Th1 cells, Th17 cells, myeloid cell infiltration, IL-12, interferon-gamma, IL-27, cytokine regulation
MeSH terms: Animals, Cells, Cultured, Encephalomyelitis, Autoimmune, Experimental, Female, Flow Cytometry, Glycoproteins, T-Lymphocytes, Helper-Inducer, Interferon-gamma, Interleukins, Male, Mice, Inbred C57BL, Mice, Inbred Strains, Mice, Transgenic, Peptide Fragments, Granulocyte-Macrophage Colony-Stimulating Factor, Mice, Knockout, Th1 Cells, Interleukin-12, Interleukin-17, Mice, Interleukin-23, Nuclear Receptor Subfamily 1, Group F, Member 3, Th17 Cells, Myelin-Oligodendrocyte Glycoprotein

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review

RORγt drives production of the cytokine GM-CSF in helper T cells, which is essential for the effector phase of autoimmune neuroinflammation

Abstract

Overview

Integrity signals

Verification

Claims the paper makes

Claims other papers make about this one

Citations

Cites

Cited by

Related

Metadata

Record

About these checks