Environmental cues such as the day–night cycle or stressors trigger the production of glucocorticoids (GCs) by the adrenal cortex. GCs are well known for their anti-inflammatory effects that suppress the production of inflammatory cytokines and induce the apoptosis of lymphocytes. Recent studies in mice, however, have revealed pro-inflammatory effects. The diurnal oscillation of GCs induces the expression of IL-7 receptor α (IL-7Rα) and C–X–C motif chemokine receptor 4 (CXCR4) at the active phase, which drives the diurnal homing of T cells into lymphoid organs. This accumulation of T cells at the active phase enhances T-cell priming against bacterial infection and antigen immunization, leading to an increase of effector CD8 T cells and antibody production. GCs induced by moderate stress trigger the homing of memory CD8 T cells into the bone marrow and support the maintenance and response of these cells. Thus, endogenous GCs have a self-defense function to enhance adaptive immune responses. By contrast, strong stress induces even higher GC levels and causes chronic inflammation and autoimmunity. Because GCs can enhance the differentiation and function of T-helper 2 (T_h2) and T_h17 cells, high stress-induced GC levels might enhance inflammation via T_h17 cell differentiation. Overall, the positive and negative effects of GCs may regulate the balance between normal immune responses and susceptibility to infections and inflammatory diseases.

中文翻译：

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糖皮质激素对昼夜循环和压力的免疫增强作用。

昼夜循环或压力源等环境因素会触发肾上腺皮质产生糖皮质激素 (GC)。GCs以其抗炎作用而闻名，其抑制炎性细胞因子的产生并诱导淋巴细胞凋亡。然而，最近对小鼠的研究揭示了促炎作用。GCs 的昼夜振荡诱导 IL-7 受体 α (IL-7Rα) 和 C-X-C 基序趋化因子受体 4 (CXCR4) 在活跃期的表达，从而驱动 T 细胞昼夜归巢到淋巴器官中。T 细胞在活跃期的这种积累增强了 T 细胞对细菌感染和抗原免疫的启动，导致效应 CD8 T 细胞和抗体产生的增加。中等压力诱导的 GC 触发记忆 CD8 T 细胞归巢到骨髓中，并支持这些细胞的维持和反应。因此，内源性 GCs 具有自我防御功能以增强适应性免疫反应。相比之下，强烈的压力会导致更高的 GC 水平，并导致慢性炎症和自身免疫。因为 GCs 可以增强 T-helper 2 (T_h 2) 和_Th 17 细胞，高应激诱导的 GC 水平可能通过 T _h 17 细胞分化增强炎症。总体而言，GCs 的正面和负面影响可能会调节正常免疫反应与感染和炎症疾病易感性之间的平衡。