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A gradient of glucocorticoid sensitivity among helper T cell cytokines
Institution:1. Department of Cardiology, Qilu Hospital of Shandong University School of Medicine, Jinan 250012, PR China;2. Department of Cardiology, Liaocheng People''s Hospital, Clinical School of Taishan Medical University, Liaocheng 252000, PR China;3. Department of General Internal Medicine, Affiliated Hospital of Shandong University of Traditional Chinese Medicine, Jinan 250014, PR China;4. School of Biomedical Sciences, Charles Sturt University, Wagga Wagga, NSW 2678, Australia;1. Shanghai Key Laboratory for Bone and Joint Diseases, Shanghai Institute of Orthopaedics and Traumatology, Shanghai Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, China;2. Department of Orthopedics, Changzheng Hospital, Second Military Medical University of China, Shanghai, China
Abstract:Helper T (Th) cells secret specific cytokines that promote immune responses whereas glucocorticoids limit the extent of immune responses by inhibiting cytokine secretion and other functions of Th cells. However, glucocorticoid resistance develops in subgroups of patients with Th cell-driven diseases such as asthma and Crohn’s disease. Recent evidence supports that Th1, Th2, and Th17 cells have distinct glucocorticoid sensitivity. Th1 cells are sensitive to glucocorticoid-induced apoptosis and cytokine suppression while Th2 cells are sensitive to the latter but not the former and Th17 cells are resistant to both. This gradient of glucocorticoid sensitivity of Th cells corresponds to the glucocorticoid sensitivity of the diseases they underlie. We identify the mechanisms contributing to distinct glucocorticoid sensitivity of Th cells and their cytokines in the literature, as this information is useful to improve treatment strategies for glucocorticoid resistant immunological disorders.
Keywords:Glucocorticoid  Th1  Th2  Th17  IL-17
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