Signals through membrane Ig of peritoneal CD5 B cells to suppress LPS-induced Ig secretion

Murine peritoneal CD5 B cells include many B cells reactive with bromelain-treated mouse RBC (BrMRBC). Anti-BrMRBC B cells are through to expand after selection by self-antigens, but little is known about signals through their membrane Ig (mIg). Most anti-BrMRBC antibodies use VH11 and V kappa 9 genes, and VH11/V kappa 9-type antibodies are detectable specifically with rabbit anti-idiotype antibodies (here referred to as RAIa). Preincubation of peritoneal cells with RAIa at 37 degrees C before LPS stimulation reduced LPS-induced secretion of RAIa-detectable Ig. To render RAIa-reactive B cells hyporesponsive, a continuous reaction of their mIg with RAIa was necessary. Binding of BrMRBC to RAIa-reactive B cells hardly affected their LPS reactivity. It appears that fresh mIg deliver the suppressive signals after reacted with RAIa, and the degree of hyporesponsiveness of a RAIa-reactive B cell depends on the amount of mIg-RAIa complexes. RAIa-suppressed B cells could regenerate mIg in the absence of RAIa and could respond to LPS to enlarge. It is suggested that binding of RAIa to mIg renders RAIa-reactive B cells without proliferation in an anergy state, where synthesis of secretory Ig is rather specifically suppressed.