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

Exposure to stressors effects various aspects of immune function, incl uding the in vivo antibody response. We have previously reported that rats exposed to an acute session of inescapable tail shock (IS) show l ong-term reductions in anti-KLH (keyhole limpet hemocyanin) IgM and Ig G. The mechanisms responsible for this suppression are currently unkno wn. Previous work has suggested changes in CD4(+) T cells could be imp ortant. We report here that exposure to IS results in a reduction in C on A-stimulated IFN-gamma levels in mesenteric lymphocytes and splenoc ytes taken immediately after IS termination. In addition, IS exposure prevents the KLH-induced increase in the number of CD45RC(+)CD4(+) T c ells (Thl-like) in both the mesenteric lymph nodes and the spleen 4 da ys after immunization. The failure of KLH to expand the CD45RC(+)CD4() subset could be due to the stress-induced reduction in LFN-gamma lev els reported in cells taken at the time of immunization. Implications of these findings as a mechanism for the decrease in the in vivo antib ody response previously reported is discussed. (C) 1995 Academic Press , inc.