M. Fleshner et al., STRESS-INDUCED REDUCTION IN THE RAT MIXED LYMPHOCYTE-REACTION IS DUE TO MACROPHAGES AND NOT TO CHANGES IN T-CELL PHENOTYPES, Journal of neuroimmunology, 56(1), 1995, pp. 45-52
Exposure to aversive events or stressors modulates various aspects of
immune function. We have previously reported that exposure to an acute
stressor, inescapable tail shock (IS), resulted in a shift in T cell
subpopulations in rat mesenteric lymph nodes but not in cervical lymph
nodes (Fleshner et al. (1992) J. Neuroimmunol. 41, 131-142). The mese
nteric CD4(+)/CD8(+) ratio was increased immediately after exposure to
IS and was due primarily to an increase in the percent of CD4(+) cell
s. The present experiments were designed to determine the relationship
between the IS-associated phenotypic shift and its significance in th
e function of CD4(+) T cells. The function assessed was the in vitro p
roliferative response to alloantigens coded for by the Major Histocomp
atibility Complex (MHC). Using the mixed lymphocyte reaction (MLR), we
report that exposure to IS resulted in a decrease in the MLR response
of cells from both cervical and mesenteric lymph nodes. Depletion of
macrophages (nylon wool adherent cells) eliminated the IS-induced redu
ction and co-culture of macrophages (irradiation-insensitive cells) fr
om shocked rats produced the suppression. One interpretation of these
data is that exposure to IS resulted in the activation of macrophages
and the release of a suppressive factor which reduced the MLR response
of peripheral lymph node lymphocytes.