BIOCHEMICAL-MECHANISMS OF STRESS-INDUCED IMPAIRMENT OF RAT T-CELL MITOGENESIS

被引：6

作者：

HALPER, JP ^{[1
]}

MILLER, AH ^{[1
]}

TRESTMAN, RL ^{[1
]}

SANTUCCI, AC ^{[1
]}

LACKNER, C ^{[1
]}

STEIN, M ^{[1
]}

机构：

[1] CUNY MT SINAI SCH MED, DEPT PSYCHIAT, NEW YORK, NY 10029 USA

来源：

JOURNAL OF NEUROIMMUNOLOGY | 1991年 / 32卷 / 03期

关键词：

STRESS; LYMPHOCYTE; SIGNAL TRANSDUCTION; PROTEIN KINASE-C; INTRACELLULAR CALCIUM; PHORBOL ESTER; CALCIUM IONOPHORE;

D O I：

10.1016/0165-5728(91)90194-C

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Splenic mononuclear cells isolated from rats exposed to two brief stressors (5 min of restraint or 2 min of footshock) showed a diminished response to the T cell mitogens, concanavalin A and phytohemagglutinin. Cells from these stressed animals also exhibited a diminished response to stimulation with the phorbol ester, tetradecanoylphorbol acetate (TPA), and/or the calcium ionophore, ionomycin. Since stimulation with these latter two agents mimics early signals generated by mitogen surface receptor binding including increased intracellular calcium and protein kinase C activation, the data indicate that stress-related defects in T cell proliferation occur at sites other than or in addition to these early events in cellular activation.

引用

页码：241 / 247

页数：7

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