Glucocorticoid-resistant Th17 cells are selectively attenuated by cyclosporine A.

ABSTRACT: Glucocorticoids remain the cornerstone of treatment for inflammatory conditions, but their utility is limited by a plethora of side effects. One of the key goals of immunotherapy across medical disciplines is to minimize patients' glucocorticoid use. Increasing evidence suggests that variations in the adaptive immune response play a critical role in defining the dose of glucocorticoids required to control an individual's disease, and Th17 cells are strong candidate drivers for nonresponsiveness [also called steroid resistance (SR)]. Here we use gene-expression profiling to further characterize the SR phenotype in T cells and show that Th17 cells generated from both SR and steroid-sensitive individuals exhibit restricted genome-wide responses to glucocorticoids in vitro, and that this is in

SUBMITTER: Schewitz-Bowers LP 

PROVIDER: S-EPMC4386391 | biostudies-literature | 2015 Mar

REPOSITORIES: biostudies-literature