Chronic psychosocial stress promotes systemic immune activation and the development of inflammatory Th cell responses

摘要: Recent studies indicate that chronic psychosocial stress favors the development of generalized immune dysfunction. During stressor exposure neuroendocrine factors affect numbers and functionality leukocytes. However, exact mechanisms leading to systemic changes in functions during are still not clear. subordinate colony housing, a model stress, mice developed spontaneous colonic inflammation. Decreased glucocorticoid signaling, induced by combination adrenal insufficiency resistance, was thought prevent tempering local cells, promote tissue In this study we investigated status after housing analyzed potential underlying those alterations. Analysis T helper cell subsets peripheral lymph nodes revealed reduction regulatory accompanied increased effector functions. Generalized activation cells shown elevated cytokine production upon stimulation. addition, observed no apparent shift towards type 2 responses. It is likely, previously reported hypocorticism led steady inflammatory Th1, Th2, Th17 cytokines obstructed an anti-inflammatory response. conclusion, established as investigate outcome on status. We also provide evidence distinct subtypes react differentially suppressive effect glucocorticoids.