STRESSED RATS FAIL TO EXPAND THE CD45RC(+)CD4(+) (TH1-LIKE) T-CELL SUBSET IN RESPONSE TO KLH - POSSIBLE INVOLVEMENT OF IFN-GAMMA

被引:36
作者
FLESHNER, M [1 ]
HERMANN, J [1 ]
LOCKWOOD, LL [1 ]
LAUDENSLAGER, ML [1 ]
WATKINS, LR [1 ]
MAIER, SF [1 ]
机构
[1] UNIV COLORADO, HLTH SCI CTR, DEPT PSYCHIAT, BOULDER, CO 80309 USA
关键词
D O I
10.1006/brbi.1995.1011
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Exposure to stressors effects various aspects of immune function, including the in vivo antibody response. We have previously reported that rats exposed to an acute session of inescapable tail shock (IS) show long-term reductions in anti-KLH (keyhole limpet hemocyanin) IgM and IgG. The mechanisms responsible for this suppression are currently unknown. Previous work has suggested changes in CD4(+) T cells could be important. We report here that exposure to IS results in a reduction in Con A-stimulated IFN-gamma levels in mesenteric lymphocytes and splenocytes taken immediately after IS termination. In addition, IS exposure prevents the KLH-induced increase in the number of CD45RC(+)CD4(+) T cells (Thl-like) in both the mesenteric lymph nodes and the spleen 4 days after immunization. The failure of KLH to expand the CD45RC(+)CD4(+) subset could be due to the stress-induced reduction in LFN-gamma levels reported in cells taken at the time of immunization. Implications of these findings as a mechanism for the decrease in the in vivo antibody response previously reported is discussed. (C) 1995 Academic Press, inc.
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页码:101 / 112
页数:12
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