IL-4 and IL-2 selectively rescue Th cell subsets from glucocorticoid-induced apoptosis.

摘要: It is well established that T cell maturation and activation are negatively regulated by a mechanism termed apoptosis. We now present evidence glucocorticoids, known to possess immunosuppressive properties, cause apoptosis in mature Th cells, similarly what has been reported for thymocytes. cells treated with the synthetic glucocorticoid dexamethasone show genome fragmentation into oligonucleosomal fragments, proliferation of growth factor stimulated inhibited glucocorticoids. IL-4 specifically rescues Th2 from dexamethasone-mediated apoptosis, whereas IL-2 IL-1 ineffective these cells. However, relevant rescue-factor glucocorticoid-treated Th1 The rescue induced thought be mediated protein kinases (possibly kinase C), as evidenced fact inhibitor H7 blocks action Our vitro data can protected their own factors deleterious effects dexamethasone, suggest specific interactions occur between lymphokines naturally produced glucocorticoids vivo, which may play role regulation immune response.