|
|
||||||||
The Journal of Immunology, Vol 130, Issue 5 2022-2026, Copyright © 1983 by American Association of Immunologists
ARTICLES |
T Saito-Taki and M Nakano
The effect of heat-aggregated immunoglobulin G's (HAgg-IgGs) on bacterial lipopolysaccharide- (LPS) induced polyclonal B cell activation (PBA) was studied. HAgg-IgGs (10 micrograms/ml or more) that were added to cultures of spleen cells obtained from BALB/c mice remarkably decreased the numbers of anti-trinitrophenyl (TNP) antibody- producing cells (APC) generated by LPS in cultures. This suppressive effect was seen when HAgg-IgGs were added within 1 hr after the initiation of culture. Later addition of HAgg-IgGs did not cause any effective suppression of the generation of APC. Moreover, the spleen cells, which had been pretreated with HAgg-IgGs, washed for removal of free HAgg-IgGs, and subsequently cultured, responded poorly to LPS. HAgg-IgG2b was more effective than HAgg-IgGs, but HAgg-IgG2a did not have any suppressive effect. A similar suppressive effect was observed when HAgg-IgG2b-Fc was added into culture, whereas none was noted with IgG2b-Fab. Indomethacin (IM), known as cyclooxygenase inhibitor, could completely abrogate the suppressive effects of HAgg-IgGs on LPS-induced PBA responses when it was added to the cell cultures together with HAgg- IgGs or to the cultures of HAgg-IgGs-pretreated cells. Addition of prostaglandin E2 (PGE2) showed strong suppression of the PBA responses of spleen cell cultures that had been pretreated with HAgg-IgGs and IM, but other PG analogues showed no suppression. Thus, it would appear that PGE2 has some role in the suppression of the LPS-induced PBA response.
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |