INDUCTION OF CD45 ISOFORM SWITCH IN MURINE B-CELLS BY ANTIGEN RECEPTOR STIMULATION AND BY PHORBOL-MYRISTATE ACETATE AND IONOMYCIN

In this study, we examined whether CD45 isoform can be switched in murine mature B cells and what signals are responsible for the process. Stimulation of murine splenic B cells with lipopolysaccharide did not reduce the expression of CD45RA-, B-, and C-exon-dependent epitopes or a CD45 common epitope, but rather enhanced the expression. Stimulation with goat anti-mouse IgM antibody did not significantly reduce CD45 expression but caused a partial reduction in the expression of CD45RA-, B-, and C-exon-dependent epitopes. Phorbol myristate acetate (PMA) alone did not significantly alter the expression of CD45 but the combination of PMA and ionomycin induced a strong reduction in the expression of CD45RA-, B-, and C-exon-dependent epitopes without affecting the level of CD45 common epitope expression. Reverse transcription and polymerase chain reaction analysis demonstrated that CD45 isoform switch induced by anti-IgM or PMA plus ionomycin is indeed mediated by alternative splicing of A-, B-, and C-exon-derived mRNA. These results suggest that CD45 isoform of murine mature B cells can be switched by antigen receptor-mediated signals, and the process seems to be regulated at least in part by protein kinase C activation and mobilization of calcium ions. © 1993 Academic Press, Inc.