Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A
2015; National Academy of Sciences; Volume: 112; Issue: 13 Linguagem: Inglês
10.1073/pnas.1418316112
ISSN1091-6490
AutoresLauren P. Schewitz‐Bowers, Philippa J P Lait, David A. Copland, Ping Chen, Wenting Wu, Ashwin Dhanda, Barbara P. Vistica, Emily L. Williams, Baoying Liu, Shayma Jawad, Zhiyu Li, William R Tucker, Sima Hirani, Yoshiyuki Wakabayashi, Jun Zhu, Nida Sen, Becky Conway-Campbell, Igal Gery, Andrew D. Dick, Lai Wei, Robert B. Nussenblatt, Richard Lee,
Tópico(s)Immunotherapy and Immune Responses
ResumoSignificance Cyclosporine A was one of the first drugs used in clinical practice to successfully rescue glucocorticoid-resistant inflammatory diseases. In this article we extend the characterization of glucocorticoid-resistant human Th17 cells, and demonstrate that this effector memory T-cell subset is reciprocally attenuated by cyclosporine A. This therapeutic paradigm was confirmed in a murine model of autoimmunity, refining our understanding of cyclosporine A’s effect on the adaptive immune response. These data support the rationale for Th17-targeting therapies in the treatment of glucocorticoid-resistant inflammation.
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