The DOI matches its Crossref record; 17 of the 17 references it cites were found in a registry or an index.
Modulation of Innate and Adaptive Immune Responses by Tofacitinib (CP-690,550)
Open accessAbstract
Inhibitors of the JAK family of nonreceptor tyrosine kinases have demonstrated clinical efficacy in rheumatoid arthritis and other inflammatory disorders; however, the precise mechanisms by which JAK inhibition improves inflammatory immune responses remain unclear. In this study, we examined the mode of action of tofacitinib (CP-690,550) on JAK/STAT signaling pathways involved in adaptive and innate immune responses. To determine the extent of inhibition of specific JAK/STAT-dependent pathways, we analyzed cytokine stimulation of mouse and human T cells in vitro. We also investigated the consequences of CP-690,550 treatment on Th cell differentiation of naive murine CD4+ T cells. CP-690,550 inhibited IL-4–dependent Th2 cell differentiation and interestingly also interfered with Th17 cell differentiation. Expression of IL-23 receptor and the Th17 cytokines IL-17A, IL-17F, and IL-22 were blocked when naive Th cells were stimulated with IL-6 and IL-23. In contrast, IL-17A production was enhanced when Th17 cells were differentiated in the presence of TGF-β. Moreover, CP-690,550 also prevented the activation of STAT1, induction of T-bet, and subsequent generation of Th1 cells. In a model of established arthritis, CP-690,550 rapidly improved disease by inhibiting the production of inflammatory mediators and suppressing STAT1-dependent genes in joint tissue. Furthermore, efficacy in this disease model correlated with the inhibition of both JAK1 and JAK3 signaling pathways. CP-690,550 also modulated innate responses to LPS in vivo through a mechanism likely involving the inhibition of STAT1 signaling. Thus, CP-690,550 may improve autoimmune diseases and prevent transplant rejection by suppressing the differentiation of pathogenic Th1 and Th17 cells as well as innate immune cell signaling.
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Cites
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IL-23 drives a pathogenic T cell population that induces autoimmune inflammation
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A quantitative analysis of kinase inhibitor selectivity
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IL-17 plays an important role in the development of experimental autoimmune encephalomyelitis
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Cited by
The JAK/STAT signaling pathway: from bench to clinic
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JAK inhibition as a therapeutic strategy for immune and inflammatory diseases
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Self-citationThe role of JAK/STAT signaling pathway and its inhibitors in diseases.
Xin, P., Xu, X., Deng, C., Liu, S., Wang, Y., Zhou, X., Ma, H., Wei, D., & Sun, S. (2020) · International Immunopharmacology · doi:10.1016/j.intimp.2020.106210 · Cited by 1,010
Alopecia areata is driven by cytotoxic T lymphocytes and is reversed by JAK inhibition
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Metadata
- Authors
- Ghoreschi, K., Jesson, M. I., Li, X., Lee, J. L., Ghosh, S., Alsup, J. W., Warner, J. D., Tanaka, M., Steward-Tharp, S. M., Gadina, M., Thomas, C. J., Minnerly, J. C., Storer, C. E., LaBranche, T. P., Radi, Z. A., Dowty, M. E., Head, R. D., Meyer, D. M., Kishore, N., & O’Shea, J. J.
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-04-01
- Volume
- 186
- Issue
- 7
- Pages
- 4234-4243
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W2121219094
- Cited by
- 645
- References
- 17
- FWCI
- 19.72
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Ghoreschi, K., Jesson, M. I., Li, X., Lee, J. L., Ghosh, S., Alsup, J. W., Warner, J. D., Tanaka, M., Steward-Tharp, S. M., Gadina, M., Thomas, C. J., Minnerly, J. C., Storer, C. E., LaBranche, T. P., Radi, Z. A., Dowty, M. E., Head, R. D., Meyer, D. M., Kishore, N., & O’Shea, J. J. (2011). Modulation of Innate and Adaptive Immune Responses by Tofacitinib (CP-690,550). The Journal of Immunology. https://doi.org/10.4049/jimmunol.1003668
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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
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