Signals through Membrane Ig of Peritoneal CD5 B Cells to Suppress LPS-Induced Ig Secretion

Abstract

Murine peritoneal CD5 B cells include many B cells reactive with bromelain-treated mouse RBC (BrMRBC). Anti-BrMRBC B cells are thought 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 Vk9 genes, and VH11/Vk9-type antibodies are detectable specifically with rabbit anti-idiotype antibodies (here referred to as RAIa). Preincubation of peritoneal cells with RAIa at 37°C before LPS stimulation reduced LPS-induced secretion of RAIn-detectable Ig. To render RAIn-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 RAIn-reactive B cells without proliferation in an anergy state, where synthesis of secretory Ig is rather specifically suppressed.