Ru486 blocks the differentially suppressive effect of stress on the
in vivo anti-klh igm, igg, igg1, and igg2a response.
Fleshner, M., F. X. Brennan, K., Ngyen, L. R. Watkins & S. F.
Maier.
Department of Psychology, University of Colorado-Boulder, Boulder,
CO 80309, Department of Psychology, Wilkes University, Wilkes-Barre,
PA 18766
APStracts 3:0212R, 1996.
Exposure to stressors can affect various aspects of immune function,
including the 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, and a failure to expand Th1-like cells in response to KLH. To
further investigate the potential role of decreased Th1-like cells in
the IS-induced reduction of anti-KLH Ig, we examined two isotypes of
IgG, IgG1 and IgG2a. Isotype switching is under cytokine control. IL
-4 helps B cells switch from making IgM to making IgG1, whereas IFN
-[gamma] helps B cells switch from making IgM to making IgG2a. In this
paper we report that IS exposure reduces IFN-[gamma] levels four days
after exposure to IS + KLH compared to immunized home cage controls.
In addition, IS exposure reduced the Th1 cytokine-sensitive anti-KLH
IgG2a but not Th2 cytokine-sensitive anti-KLH IgG1. This pattern of
isotype reduction suggests that a failure to expand the Th1 cell
which results in less IFN-[gamma] may contribute to the the IS
-induced reduction in anti-KLH Ig. Glucocorticoids (GCs)
differentially regulate Th1 and Th2 cells. Administration of the type
II GC receptor antagonist RU486 before IS blocked the IS-induced
suppression in anti-KLH IgM, IgG, IgG2a. Corticosterone (2.5 mg/kg),
however, did not produce the suppression in anti-KLH Ig. These
results support a role of corticosterone in mediating IS-induced
reductions in in vivo antibody.
Received 26 January 1996; accepted in final form 15 May 1996.
APS Manuscript Number R48-6.
Article publication pending Am. J. Physiol. (Regulatory Integrative
Comp. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 17 June 96