THE INTERACTION BETWEEN INTERLEUKIN-1 AND GLUCOCORTICOIDS IN THE IN-VIVO ANTIBODY-RESPONSE OF MICE TO 3 CONCENTRATIONS OF ANTIGEN

Citation
Lg. Krymskaya et al., THE INTERACTION BETWEEN INTERLEUKIN-1 AND GLUCOCORTICOIDS IN THE IN-VIVO ANTIBODY-RESPONSE OF MICE TO 3 CONCENTRATIONS OF ANTIGEN, Brain, behavior, and immunity, 8(4), 1994, pp. 327-340
Citations number
36
Categorie Soggetti
Neurosciences,Immunology
ISSN journal
08891591
Volume
8
Issue
4
Year of publication
1994
Pages
327 - 340
Database
ISI
SICI code
0889-1591(1994)8:4<327:TIBIAG>2.0.ZU;2-H
Abstract
Antigenic challenge leads to a transient increase of serum glucocortic oids, a phenomenon that has been implicated in regulation of the magni tude of the immune response. In the present study, we determined the e ffects of immunization with three different doses of the T-dependent a ntigen, sheep red blood cells (SRBC), on glucocorticoid levels, IL-I p roduction by splenic macrophages, and number of splenic antibody-formi ng cells in mice. Immunization with three doses of antigen caused a do se-dependent increase in serum glucocorticoid after 2-4 h. No effect o f immunization on serum corticosteroid-binding globulin levels was fou nd, suggesting that the concentration of free, hormonally active corti costerone was increased. Antigenic challenge resulted in a significant rise of IL-1 production in a dose-related manner 2 h after immunizati on, except for the group given the highest dose of SRBC, which demonst rated strong elevation of serum corticosterone level by this time. How ever, IL-1 production by splenic macrophages, isolated at the peak of the hormonal reaction to SRBC (4 h after immunization), was suppressed in a dose-dependent fashion. An inverse relationship between endogeno us levels of glucocorticoids and splenic plaque-forming cells number w as also revealed. It is concluded that the interaction of IL-1 and glu cocorticoids during the first hours after antigenic challenge is one o f the factors controlling the magnitude of the immune response. (C) 19 94 Academic Press, Inc.