The DOI matches its Crossref record; 53 of the 53 references it cites were found in a registry or an index.
IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice
Open accessAbstract
Psoriasis is a common chronic autoimmune skin disease of unknown cause that involves dysregulated interplay between immune cells and keratinocytes. IL-22 is a cytokine produced by the TH1, TH17, and TH22 subsets that are functionally implicated in the psoriatic pathology. We assessed the role of IL-22 in a mouse model where psoriasiform skin inflammation is triggered by topical application of the TLR7/8 agonist imiquimod. At the macroscopic level, scaly skin lesions induced by daily applications of imiquimod in wild-type mice were almost totally absent in IL-22–deficient mice or in mice treated with a blocking anti–IL-22 Ab. At the microscopic level, IL-22–deficient mice showed a dramatic decrease in the development of pustules and a partial decrease in acanthosis. At the molecular level, the absence or inhibition of IL-22 strongly decreased the expression of chemotactic factors such as CCL3 and CXCL3 and of biomarkers such as S100A8, S100A7, and keratin 14, which reflect the antimicrobial and hyperproliferative responses of keratinocytes. IL-22 also played a major role in neutrophil infiltration after imiquimod treatment. IL-23 was required for IL-22 production, and γδ TCR lymphocytes represented the major source of IL-22 in lymph nodes from imiquimod-treated mice. However, T cells were not absolutely required for IL-22 production because imiquimod-induced IL-22 expression in the skin is still preserved in Rag2−/− mice. Taken together, our data show that IL-22 is required for psoriasis-like lesions in the mouse imiquimod model and is produced by both T cells and innate immune cells.
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Self-citationImiquimod-Induced Psoriasis-Like Skin Inflammation in Mice Is Mediated via the IL-23/IL-17 Axis
van der Fits, L., Mourits, S., Voerman, J. S. A., Kant, M., Boon, L., Laman, J. D., Cornelissen, F., Mus, A.-M., Florencia, E., Prens, E. P., et al. (2009) · The Journal of Immunology · doi:10.4049/jimmunol.0802999 · Cited by 2,176
Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis
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Pathogenesis and therapy of psoriasis
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IL-22 Increases the Innate Immunity of Tissues
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γδ T cell effector functions: a blend of innate programming and acquired plasticity
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Cited by
Six-of-the-best: unique contributions of γδ T cells to immunology
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T cell subsets and their signature cytokines in autoimmune and inflammatory diseases
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The IL-23/T17 pathogenic axis in psoriasis is amplified by keratinocyte responses
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Rorγt+ innate lymphocytes and γδ T cells initiate psoriasiform plaque formation in mice
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Activation of the Aryl Hydrocarbon Receptor Dampens the Severity of Inflammatory Skin Conditions
Di Meglio, P., Duarte, J. H., Ahlfors, H., Owens, N. D. L., Li, Y., Villanova, F., Tosi, I., Hirota, K., Nestle, F. O., Mrowietz, U., et al. (2014) · Immunity · doi:10.1016/j.immuni.2014.04.019 · Cited by 373
Metadata
- Authors
- Van Belle, A. B., de Heusch, M., Lemaire, M. M., Hendrickx, E., Warnier, G., Dunussi-Joannopoulos, K., Fouser, L. A., Renauld, J.-C., & Dumoutier, L.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2012-01-01
- Volume
- 188
- Issue
- 1
- Pages
- 462-469
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2155582127
- Cited by
- 287
- References
- 53
- FWCI
- 10.19
- Type
- journal article
- Language
- en
- Open access
- green
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- Van Belle, A. B., de Heusch, M., Lemaire, M. M., Hendrickx, E., Warnier, G., Dunussi-Joannopoulos, K., Fouser, L. A., Renauld, J.-C., & Dumoutier, L. (2012). IL-22 Is Required for Imiquimod-Induced Psoriasiform Skin Inflammation in Mice. The Journal of Immunology. https://doi.org/10.4049/jimmunol.1102224
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