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Macrophages and neutrophils are the targets for immune suppression by glucocorticoids in contact allergy
Open accessAbstract
Glucocorticoids (GCs) are widely used in the treatment of allergic skin conditions despite having numerous side effects. Here we use Cre/loxP-engineered tissue- and cell-specific and function-selective GC receptor (GR) mutant mice to identify responsive cell types and molecular mechanisms underlying the antiinflammatory activity of GCs in contact hypersensitivity (CHS). CHS was repressed by GCs only at the challenge phase, i.e., during reexposure to the hapten. Inactivation of the GR gene in keratinocytes or T cells of mutant mice did not attenuate the effects of GCs, but its ablation in macrophages and neutrophils abolished downregulation of the inflammatory response. Moreover, mice expressing a DNA binding-defective GR were also resistant to GC treatment. The persistent infiltration of macrophages and neutrophils in these mice is explained by an impaired repression of inflammatory cytokines and chemokines such as IL-1beta, monocyte chemoattractant protein-1, macrophage inflammatory protein-2, and IFN-gamma-inducible protein 10. In contrast TNF-alpha repression remained intact. Consequently, injection of recombinant proteins of these cytokines and chemokines partially reversed suppression of CHS by GCs. These studies provide evidence that in contact allergy, therapeutic action of corticosteroids is in macrophages and neutrophils and that dimerization GR is required.
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“This hypothesis is supported by prior work showing that repression of IL-1β, MIP-2, MCP-1, and IP-10 by GCs is hindered in macrophages isolated from GRdim mice (109, 110).”
From The HPA – Immune Axis and the Immunomodulatory Actions of Glucocorticoids in the Brain (2014) · cites this paper as [110]
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BackgroundThe role of the glucocorticoid receptor in inflammation and immunity
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Tumor-Induced IL-6 Reprograms Host Metabolism to Suppress Anti-tumor Immunity
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“Deletion of NR3C1, the glucocorticoid receptor, in these cells has been shown to abolish glucocorticoid-dependent suppression of the expression of Cxcl10 and other chemotactic factors in a contact hypersensitivity reaction (Tuckermann et al., 2007).”
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Glucocorticoids—All-Rounders Tackling the Versatile Players of the Immune System
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“In contrast, GR mice were refractory to GC treatment in a mouse model of contact hypersensitivity, which mimics allergic contact dermatitis (58).”
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BackgroundCrosstalk between the glucocorticoid receptor and other transcription factors: Molecular aspects
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“Moreover, a recent report showed an impaired GC-mediated repression of some inflammatory cytokines and chemokines in macrophages derived from GR mice (Tuckermann et al., 2007).”
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Glucocorticoids sensitize the innate immune system through regulation of the NLRP3 inflammasome
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“…et al. 2011) Inhibition of irritant skin inflammation (Reichardt et al. 2001) Suppression of lung injury (Vettaroazzi et al. 2015) Suppression of contact allergy (Tuckermann et al. 2007) Suppression of septic shock (Kleiman et al. 2012) (Vandevyver et al. 2012) (Silverman et al. 2013) G R Pol…”
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InfluentialRos-Bernal, F., Hunot, S., Herrero, M. T., Parnadeau, S., Corvol, J.-C., Lu, L., Alvarez-Fischer, D., Carrillo-de Sauvage, M. A., Saurini, F., Coussieu, C., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1017820108 · Cited by 231
“To elucidate precisely the neuronal versus glial role of GR in DN injury, we produced mice by Cre/loxP technology that carried selective inactivation of GR gene either in macrophages (GR mice) (17) or in DNs (GR mice) (18).”
MethodSelf-citationSelective glucocorticoid receptor modulation: New directions with non-steroidal scaffolds
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“contact allergy (Tuckermann et al., 2007) and systemic TNF-induced lethal shock (Vandevyver et al.”
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“On the other hand, they proved insensitive to therapeutic effects of GC in experimental models of contact allergy (Tuckermann et al., 2007) and arthritis (Baschant et al.”
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“These findings indicate that GR homodimerization is required for GCs to exert their anti-inflammatory effects on their main targets, which are macrophages and neutrophils (122).”
BackgroundMore Than Suppression: Glucocorticoid Action on Monocytes and Macrophages
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“Moreover, in contrast to irritant contact dermatitis GCsmediated the suppression of allergic contact dermatitis is abolished in GRdim mice (43).”
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“T cell-specific ablation of NR3C1 has been reported, although Cre recombinase activity occurs early in T-cell development and prevents discriminating the contribution of glucocorticoid signaling among T cell subtypes [91].”
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“GC suppression of contact allergy, arthritis, and allergic asthma was abrogated in GRdim mice, while this was not the case for the therapeutic effect of GCs in EAE [8,33,141,191].”
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“However, recent studies in contact hypersensitivity, a model for contact dermatitis and thus an inflammatory type of a different mechanism revealed that more than transrepression of the GR is required for suppression of inflammation (Tuckermann et al., 2007).”
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“In contrast, we had found that the dimerization-competent GR was required for anti-inflammatory effects of dex on contact allergy (18).”
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“inflammation when given GC therapy (136, 137, 139, 140).”
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Glucocorticoid receptor dimerization induces MKP1 to protect against TNF-induced inflammation
Vandevyver, S., Dejager, L., Bogaert, T. V., Kleyman, A., Liu, Y., Tuckermann, J. P., & Libert, C. (2012) · Journal of Clinical Investigation · doi:10.1172/jci60006 · Cited by 133
“Some studies have provided evidence that induction of antiinflammatory genes by GR dimers is indispensable for the antiinflammatory effects of GR (23).”
Progress and challenges of selective Farnesoid X Receptor modulation
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Glucocorticoid Signaling in Health and Disease: Insights From Tissue-Specific GR Knockout Mice
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“promoter did not sensitize these mice to contact hy persensitivity and dexamethasone was effective in reducing inflammation, indicating that the mechanism of GR-mediated inflammation in response to a dermal irritant is specific to the stimulus (30).”
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“Materials and Methods Mice Mice with conditional inactivation of GR gene: The Nr3C1loxp/loxp;LysMCre/þ (thereafter denominated GR) and Nr3C1;Tg:LckCre (thereafter denominated GR) mice were generated by crossing Nr3C1 mice(52) with LysMCre and LckCre transgenic mice, which express Cre recombinase inserted by homologous…”
MethodNeuroendocrine factors alter host defense by modulating immune function
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“A recent study reported that monocytes, along with neutrophils, are the primary targets of glucocorticoids in diminishing contact hypersensitivity reactions, as evidenced by repression of their cytokine and chemokine production [40].”
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“In murine models for contact allergy and septic shock it has been shown that the anti-inflammatory effect of glucocorticoids depends on the presence of GR in macrophages, suppressing the induction of pro-inflammatory mediators such as IL-1 β (Kleiman et al., 2012; Tuckermann et al., 2007).”
InfluentialEffects of Glucocorticoids in the Immune System
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“Macrophages Activation of JNK and p38 MAPK are inhibited, expression of pro infl ammatory genes are attenuated, contact hypersensitivity is suppressed [ 57 , 61 , 62 ]”
BackgroundInfluentialIron Regulatory Proteins Mediate Host Resistance to Salmonella Infection
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“On the other hand, myeloid and airway epithelial cells have been shown to be the GC-responsive cells during contact hypersensitivity and airway inflammation, respectively (Klaßen et al., 2017; Tuckermann et al., 2007).”
BackgroundBaschant, U., Frappart, L., Rauchhaus, U., Bruns, L., Reichardt, H. M., Kamradt, T., Bräuer, R., & Tuckermann, J. P. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1105857108 · Cited by 106
“However, in contact hypersensitivity, dimerization and binding of the GR to DNA are necessary for the antiinflammatory effects (9).”
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“For the results in Figure 2c, 4b, 4d and Supplementary Figure 3 quantitative RT-PCR was performed as described (35).”
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“However, recent studies demonstrated that under some inflammatory conditions DNA dimer-dependent gene expression could also contribute to the antiinflammatory activities of the GR [17].”
BackgroundGlucocorticoids Shape Macrophage Phenotype for Tissue Repair
Desgeorges, T., Caratti, G., Mounier, R., Tuckermann, J. P., & Chazaud, B. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01591 · Cited by 109
“In addition, GRdim mice are also insensitive to GCs, indicating that GR dimerization, likely in macrophages, is required in this context (87).”
BackgroundDefining the role of glucocorticoids in inflammation
Ronchetti, S., Migliorati, G., Bruscoli, S., & Riccardi, C. (2018) · Clinical Science · doi:10.1042/cs20171505 · Cited by 104
Clinical Use and Molecular Action of Corticosteroids in the Pediatric Age
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“For instance, T cells are essential targets for the treatment of EAE, whereas macrophages and neutrophils are critical for control of contact dermatitis by free GC [32,33].”
BackgroundZhang, E. Y., Chen, A. Y., & Zhu, B. T. (2009) · PLoS ONE · doi:10.1371/journal.pone.0007703 · Cited by 78
“Approximately twenty-four hours after subsequent exposures to DNCB (often referred to as ‘‘challenges’’), macrophages were found to accumulate at the site of DNCB exposure [4], contributing to the development of dermatitis (e.”
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Schweingruber, N., Haine, A., Tiede, K., Karabinskaya, A., van den Brandt, J., Wüst, S., Metselaar, J. M., Gold, R., Tuckermann, J. P., Reichardt, H. M., et al. (2011) · The Journal of Immunology · doi:10.4049/jimmunol.1101604 · Cited by 76
Loss of menin in osteoblast lineage affects osteocyte–osteoclast crosstalk causing osteoporosis
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“RNA was reverse-transcribed by a cDNA kit (Applied Biosystems, Carlsbad, CA, USA) and real-time qPCR was performed as previously described.(30) Primer sequences are available upon request.”
MethodTea Polysaccharides Inhibit Colitis-Associated Colorectal Cancer via Interleukin-6/STAT3 Pathway
Liu, L. Q., Nie, S., Shen, M., Hu, J., Yu, Q., Gong, D., & Xie, M. Y. (2018) · Journal of Agricultural and Food Chemistry · doi:10.1021/acs.jafc.8b00710 · Cited by 73
From innate to adaptive immune responses in contact hypersensitivity
Martin, S. F., & Jakob, T. (2008) · Current Opinion in Allergy and Clinical Immunology · doi:10.1097/aci.0b013e3283088cf9 · Cited by 73
Stifel, U., Wolfschmitt, E.-M., Vogt, J. A., Wachter, U. A., Vettorazzi, S., Tews, D., Hogg, M., Zink, F., Koll, N., Winning, S., et al. (2021) · Molecular Metabolism · doi:10.1016/j.molmet.2021.101424 · Cited by 73
“There was also a small, but signi fi cant, reduction in macrophage nuclear HIF1 a in GR LysMCre mice treated with Dex, likely due to the known limitations of the LysM-CRE, which have around a 70% recombination rate in macrophages [14].”
Connecting the Metabolic and Immune Responses to Cancer
Flint, T. R., Fearon, D. T., & Janowitz, T. (2017) · Trends in Molecular Medicine · doi:10.1016/j.molmed.2017.03.001 · Cited by 71
Silverman, M. N., Mukhopadhyay, P., Belyavskaya, E., Tonelli, L. H., Revenis, B. D., Doran, J. H., Ballard, B. E., Tam, J., Pacher, P., & Sternberg, E. M. (2013) · Molecular Psychiatry · doi:10.1038/mp.2012.131 · Cited by 64
Neuro-consequences of the spaceflight environment
Mhatre, S. D., Iyer, J. S., Puukila, S., Paul, A. M., Tahimic, C. G. T., Rubinstein, L., Lowe, M. G., Alwood, J. S., Sowa, M. B., Bhattacharya, S., et al. (2021) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2021.09.055 · Cited by 63
Cortisol-induced immune suppression by a blockade of lymphocyte egress in traumatic brain injury
Dong, T., Liang, Z., Bhayana, B., & Wu, M. X. (2016) · Journal of Neuroinflammation · doi:10.1186/s12974-016-0663-y · Cited by 64
“The mechanism underlying its anti-inflammatory effects may be multifaceted including transcriptional suppression of proinflammatory genes [45, 46] and inhibition of the functions of macrophages and neutrophils [47], and the like.”
BackgroundRegulatory effects of dexamethasone on NK and T cell immunity
Chen, L., Jondal, M., & Yakimchuk, K. (2017) · Inflammopharmacology · doi:10.1007/s10787-017-0418-0 · Cited by 66
Topical ivermectin improves allergic skin inflammation
Ventre, E., Rozières, A., Lenief, V., Albert, F., Rossio, P., Laoubi, L., Dombrowicz, D., Staels, B., Ulmann, L., Julia, V., et al. (2017) · Allergy · doi:10.1111/all.13118 · Cited by 61
“Conversely, IVM had no major impact on the activation status of skin DC, both in vivo and in vitro, and on the migration of skin DC to regional lymph nodes, a phenomenon that is observed with other immunomodulatory drugs used in the treatment for AD, such as tacrolimus, rapamycin, and dexamethasone (27, 28).”
BackgroundKoenen, M., Culemann, S., Vettorazzi, S., Caratti, G., Frappart, L., Baum, W., Krönke, G., Baschant, U., & Tuckermann, J. P. (2018) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2017-212762 · Cited by 59
Glucocorticoid Receptor Is Required for Skin Barrier Competence
Bayo, P., Sanchís, A., Bravo, A., Cascallana, J. L., Buder, K., Tuckermann, J. P., Schütz, G., & Pérez, P. (2007) · Endocrinology · doi:10.1210/en.2007-0814 · Cited by 58
Choi, J. H., Jin, S. W., Park, B. H., Kim, H. G., Khanal, T., Han, H. J., Hwang, Y. P., Choi, J. M., Chung, Y., Hwang, S. K., et al. (2013) · Food and Chemical Toxicology · doi:10.1016/j.fct.2013.02.037 · Cited by 57
Conaway, H. H., Henning, P., Lie, A., Tuckermann, J. P., & Lerner, U. H. (2016) · Bone · doi:10.1016/j.bone.2016.08.024 · Cited by 57
Keratinocytes control skin immune homeostasis through de novo–synthesized glucocorticoids
Phan, T. S., Schink, L., Mann, J., Merk, V. M., Zwicky, P., Mundt, S., Simon, D., Kulms, D., Abraham, S., Legler, D. F., et al. (2021) · Science Advances · doi:10.1126/sciadv.abe0337 · Cited by 56
“In particular, inflammatory monocytes, macrophages, and neutrophils were shown to represent responsive targets for GC treatment in allergic contact dermatitis ( 35 ).”
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
“The following mutant mouse strains were bred in our animal facility in göttingen: gr control mice (designated gr) on a C57Bl/6 background, gr mice crossed with lckCre mice (designated gr) on a C57Bl/6 background and gr mice (designated gr) on either a C57Bl/6 or a Balb/c background [37, 47, 51].”
MethodZimmermann, G. R., Avery, W., Finelli, A. L., Farwell, M., Fraser, C. C., & Borisy, A. A. (2009) · Arthritis Research & Therapy · doi:10.1186/ar2602 · Cited by 54
“Finally, macrophages from GRdim mice exhibit a decreased potency of glucocorticoid suppression of IL-1β, monocyte chemotactic protein-1 (CCL2), macrophage inflammatory protein-2 (CXCL2), and interferon-gamma-inducible protein-10 (CXCL10) [20].”
BackgroundAirway Epithelial Cells Are Crucial Targets of Glucocorticoids in a Mouse Model of Allergic Asthma
Klaßen, C., Karabinskaya, A., Dejager, L., Vettorazzi, S., Moorleghem, J. V., Lühder, F., Meijsing, S. H., Tuckermann, J. P., Bohnenberger, H., Libert, C., et al. (2017) · The Journal of Immunology · doi:10.4049/jimmunol.1601691 · Cited by 54
“For instance, Dex application to GR mice failed to resolve inflammation in mouse models of contact allergy, arthritis, and acute lung injury (19, 20, 44).”
BackgroundMeers, G. K., Bohnenberger, H., Reichardt, H. M., Lühder, F., & Reichardt, S. D. (2018) · PLoS ONE · doi:10.1371/journal.pone.0190846 · Cited by 54
Ferring–Appel, D., Hentze, M. W., & Galy, B. (2008) · Blood · doi:10.1182/blood-2008-05-155093 · Cited by 53
Choi, J. H., Kim, H. G., Jin, S. W., Han, E. H., Khanal, T., Truong, M., Hwang, Y. P., Choi, J. M., Chun, S.-S., Chung, Y., et al. (2012) · Food and Chemical Toxicology · doi:10.1016/j.fct.2012.11.025 · Cited by 51
Glucocorticoid activation of anti-inflammatory macrophages protects against insulin resistance
Caratti, G., Stifel, U., Caratti, B., Jamil, A. J. M., Chung, K., Kiehntopf, M., Gräler, M. H., Blüher, M., Rauch, A., & Tuckermann, J. P. (2023) · Nature Communications · doi:10.1038/s41467-023-37831-z · Cited by 52
Liu, H., Zhou, L., Wang, X., Zheng, Q., Zhan, F., Zhou, L., Dong, Y., Xiong, Y., Yi, P., Guohai, X., et al. (2024) · Biochemical Pharmacology · doi:10.1016/j.bcp.2024.116050 · Cited by 55
CD163 expression defines specific, IRF8-dependent, immune-modulatory macrophages in the bone marrow
Fischer‐Riepe, L., Daber, N., Schulte-Schrepping, J., Carvalho, B. C. V. D., Russo, A., Pohlen, M., Fischer, J., Chasan, A. I., Wolf, M., Ulas, T., et al. (2020) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2020.02.034 · Cited by 48
Thymus-derived glucocorticoids mediate androgen effects on thymocyte homeostasis
Chen, Y., Qiao, S., Tuckermann, J. P., Okret, S., & Jondal, M. (2010) · The FASEB Journal · doi:10.1096/fj.10-168724 · Cited by 49
Glucocorticoids suppress Wnt16 expression in osteoblasts in vitro and in vivo
Hildebrandt, S., Baschant, U., Thiele, S., Tuckermann, J. P., Hofbauer, L. C., & Rauner, M. (2018) · Scientific Reports · doi:10.1038/s41598-018-26300-z · Cited by 51
Biological clock dysfunction exacerbates contact hypersensitivity in mice
Takita, E., Yokota, S., Tahara, Y., Hirao, A., Aoki, N., Nakamura, Y., Nakao, A., & Shibata, S. (2012) · British Journal of Dermatology · doi:10.1111/j.1365-2133.2012.11176.x · Cited by 49
Glucocorticoid receptors, epidermal homeostasis and hair follicle differentiation
Pérez, P. (2011) · Dermato-Endocrinology · doi:10.4161/derm.15332 · Cited by 45
Glucocorticoid-targeted therapies for the treatment of rheumatoid arthritis
Strehl, C., van der Goes, M. C., Bijlsma, J. W. J., Jacobs, J. W. G., & Buttgereit, F. (2017) · Expert Opinion on Investigational Drugs · doi:10.1080/13543784.2017.1276562 · Cited by 46
“these mutant mice, some inflammatory processes can be suppressed by GCs, while others cannot [74].”
BackgroundReichardt, S. D., Föller, M., Rexhepaj, R., Pathare, G., Minnich, K., Tuckermann, J. P., Lang, F. J. W., & Reichardt, H. M. (2012) · Endocrinology · doi:10.1210/en.2011-1747 · Cited by 44
Hu, L., Edamatsu, H., Takenaka, N., Ikuta, S., & Kataoka, T. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0901816 · Cited by 46
“Substantialattenuationof theinflammatoryreactions in theelicitation stage of CHS is observed in PLCe2/2 mice.”
BackgroundInfluentialSuwanpradid, J., Shih, M., Pontius, L. N., Yang, B., Birukova, A., Guttman‐Yassky, E., Corcoran, D. L., Que, L. G., Tighe, R. M., & MacLeod, A. S. (2017) · The Journal of Immunology · doi:10.4049/jimmunol.1700739 · Cited by 45
“In our mouse CHS studies, we show that MF are required at the elicitation but not the sensitization phase of CHS, which is in agreement with a recently published study (11, 12).”
BackgroundMethodResultInfluentialFenton, C. G., Martin, C., Jones, R. L., Croft, A. P., Campos, J., Naylor, A. J., TAYLOR, A. E. R., Chimen, M., Cooper, M. S., Lavery, G. G., et al. (2020) · Annals of the Rheumatic Diseases · doi:10.1136/annrheumdis-2020-218493 · Cited by 45
Galuppo, P., Vettorazzi, S., Hoevelmann, J., Scholz, C. J., Tuckermann, J. P., Bauersachs, J. K., & Fraccarollo, D. (2017) · The FASEB Journal · doi:10.1096/fj.201700317r · Cited by 42
“GRdeficiency inGRmice targetsmonocytes and neutrophils (20).”
Estradiol increases hematopoietic stem and progenitor cells independent of its actions on bone
Illing, A., Liu, P., Ostermay, S., Schilling, A. F., de Haan, G., Krust, A., Amling, M., Chambon, P., Schinke, T., & Tuckermann, J. P. (2012) · Haematologica · doi:10.3324/haematol.2011.052456 · Cited by 43
“Flow cytometry Flow cytometry was performed as described.(12) Monoclonal antibodies from Natutec /eBioscience were: Gr1-FITC, B220-FITC, CD3-FITC, CD11b-FITC, Ter119-FITC, Sca1-PE,CD117-APC, CD150-PE, CD150-APC, CD48-PE, CD48APC, CD45.”
MethodShifting Paradigms in Allergic Contact Dermatitis: The Role of Innate Immunity
Brys, A. K., Rodriguez-Homs, L. G., Suwanpradid, J., Atwater, A. R., & MacLeod, A. S. (2019) · Journal of Investigative Dermatology · doi:10.1016/j.jid.2019.03.1133 · Cited by 44
“However, recent studies have shown that innate immune cells are in fact critical moderators of the efferent phase of ACD (Natsuaki et al., 2014; Suwanpradid et al., 2017b; Tuckermann et al., 2007).”
BackgroundTheiss-Suennemann, J., Jörß, K., Messmann, J. J., Reichardt, S. D., Montes‐Cobos, E., Lühder, F., Tuckermann, J. P., AWolff, H., Dressel, R., Gröne, H., et al. (2014) · The Journal of Pathology · doi:10.1002/path.4475 · Cited by 41
“For instance, T cells are the major target of GCs in mouse models of multiple sclerosis and rheumatoid arthritis, whereas suppression of macrophages is crucial in the control of contact hypersensitivity and sepsis [9,13-16].”
BackgroundGR Dimerization and the Impact of GR Dimerization on GR Protein Stability and Half-Life
Louw, A. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.01693 · Cited by 42
“For example, in skin, inhibition of the swelling response during the challenge phase, upon re-exposure to the hapten, 2,4-dinitrofluorobenzene, by exogenous intraperitoneal or oral DEX administration in contact dermatitis, a T cell–dependent delayed-type hypersensitivity reaction, is not observed in GRdim mice (118),…”
Background
Metadata
- Authors
- Tuckermann, J. P., Kleiman, A., Moriggl, R., Spanbroek, R., Neumann, A., Illing, A., Clausen, B. E., Stride, B., Förster, I., Habenicht, A. J. R., Reichardt, H. M., Tronche, F., Schmid, W., & Schütz, G.
- Affiliations
- German Cancer Research Center (DE)
- Ludwig Boltzmann Institute for Cancer Research (AT)
- Friedrich Schiller University Jena (DE)
- Leibniz Institute on Aging - Fritz Lipmann Institute (FLI) (DE)
- Amsterdam UMC Location University of Amsterdam (NL)
- Heinrich Heine University Düsseldorf (DE)
- University of Göttingen (DE)
- Centre National de la Recherche Scientifique (FR)
- Corresponding author
- Tuckermann, Jan P.
- Schütz, Günther
- ORCID
- Venue
- Journal of Clinical Investigation
- Published
- 2007-05-01
- Volume
- 117
- Issue
- 5
- Pages
- 1381-1390
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC1849982
- OpenAlex
- W2060990402
- Cited by
- 252
- References
- 54
- Citations by year
- 2026: 5 · 2025: 5 · 2024: 9 · 2023: 13 · 2022: 12 · 2021: 16 · 2020: 17 · 2019: 17 · 2018: 18 · 2017: 16 · 2016: 15 · 2015: 11 · 2014: 14 · 2013: 11 · 2012: 20
- FWCI
- 13.87
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Pure Amsterdam UMC (publishedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Informationszentrum Lebenswissenschaften (ZB MED) (submittedVersion)
- GRO (submittedVersion)
- Funders
- Deutsches Krebsforschungszentrum (69120, D-69120)
- Landsteiner Foundation for Blood Transfusion Research
- Deutsche Forschungsgemeinschaft (SFB405, SFB 636, SFB 488)
- Bundesministerium für Bildung und Forschung (01GS0477, 01GZ0310, KGCV1, 01GS0416)
- Austrian Science Fund (SFB‐F28)
- Nederlandse Organisatie voor Wetenschappelijk Onderzoek (917.76.365)
- Leibniz-Gemeinschaft
- Topics
- Health Sciences › Medicine › Dermatology › Contact Dermatitis and Allergies
- Health Sciences › Medicine › Dermatology › Dermatology and Skin Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
- Keywords
- glucocorticoids, contact hypersensitivity, contact allergy, macrophages, neutrophils, glucocorticoid receptor, anti-inflammatory mechanism, chemokines, inflammatory cytokines, keratinocytes, T cells, skin inflammation
- MeSH terms
- Animals, Anti-Inflammatory Agents, Cells, Cultured, Dexamethasone, Immunosuppressive Agents, Macrophages, Mice, Inbred BALB C, Mice, Inbred C57BL, Mice, Transgenic, Neutrophils, Receptors, Glucocorticoid, Drug Delivery Systems, Dermatitis, Allergic Contact, Mice
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