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This analysis reveals mechanisms of glucocorticoid resistance in Th17.1 cells, suggesting implications for autoimmune disease therapies.
The non-classical population of Th17 lymphocytes polarized toward Th1 (Th17.1/ex-Th17) is currently the focus of research attention. Possessing an unique pro-inflammatory potential and the ability to overcome histohematic barriers, these cells play a key role in the pathogenesis of many inflammatory diseases, primarily autoimmune ones: they prevail in autoimmune lesions and are considered as a promising therapeutic target for these pathologies. At the same time, recent studies have shown another distinctive feature of Th1-polarized Th17 – selective resistance to glucocorticoids. Since glucocorticoids are first-line drugs in the treatment of exacerbations in autoimmune diseases, understanding the causes of this phenomenon is fundamentally important for predicting patients’ response to therapy and for improving the effectiveness of such therapy. In this paper, we analyze the mechanisms of drug resistance formation in Th17 cells polarized toward Th1, compare them with similar processes in non-pathogenic, classical Th17, and discuss the role of such resistance in the response to glucocorticoid therapy.
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E. M. Kuklina (2025) studied this question.
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