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应激调节免疫细胞中的钙动员。

Stress modulates calcium mobilization in immune cells.

作者信息

Sei Y, McIntyre T, Skolnick P, Arora P K

机构信息

Laboratory of Neuroscience, National Institute of Diabetes, Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD 20892.

出版信息

Life Sci. 1991;49(9):671-6. doi: 10.1016/0024-3205(91)90114-q.

Abstract

Both acute and chronic restraint stress modulated mitogen-induced increases in cytoplasmic free-calcium concentrations ([Ca2+]i) in mouse spleen cells. Dual-color analysis of lymphocyte subpopulations demonstrated that acute (2 hour) restraint stress suppressed mitogen-stimulated increases in [Ca2+]i in CD4+ T cells, but enhanced [Ca2+]i in CD8+ T cells. Chronic restraint stress (2 hours daily for up to 21 days) resulted in a significant suppression of mitogen-stimulated increases in [Ca2+]i in CD4+ T cells at 3 and 7 days, but not at 21 days. CD8+ T cells were unaffected by chronic stress. Chronic stress (for 7 days) had a modest suppressive effect on mitogen-induced Ca2+ responses in B cells. Within T lymphocyte subpopulations, both acute and chronic stress predominantly affected CD4+ T cells, which may induce a functional reversal of the CD4/CD8 ratios in vivo. Such a reversal could result in suppression of a variety of immune responses such as lymphocyte proliferation and antigen-specific antibody production. These findings indicate that the inhibitory effects of stress on calcium mobilization in lymphocytes may be an early event mediating stress-induced immunosuppression.

摘要

急性和慢性束缚应激均能调节丝裂原诱导的小鼠脾细胞胞质游离钙浓度([Ca2+]i)升高。淋巴细胞亚群的双色分析表明,急性(2小时)束缚应激抑制了丝裂原刺激的CD4+ T细胞中[Ca2+]i升高,但增强了CD8+ T细胞中的[Ca2+]i。慢性束缚应激(每天2小时,持续长达21天)在第3天和第7天导致丝裂原刺激的CD4+ T细胞中[Ca2+]i升高受到显著抑制,但在第21天未出现这种情况。CD8+ T细胞不受慢性应激影响。慢性应激(持续7天)对丝裂原诱导的B细胞Ca2+反应有适度抑制作用。在T淋巴细胞亚群中,急性和慢性应激主要影响CD4+ T细胞,这可能在体内诱导CD4/CD8比值的功能逆转。这种逆转可能导致多种免疫反应受到抑制,如淋巴细胞增殖和抗原特异性抗体产生。这些发现表明,应激对淋巴细胞钙动员的抑制作用可能是介导应激诱导免疫抑制的早期事件。

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