CD5+B cells: Differential capping and modulation of IgM and CD5

CD5 is associated with the B-cell antigen receptor (BcR) complex. As an approach to understanding its role in B-cell function, the authors investigated the capping and modulation of CD5 and surface IgM (sIgM). Tonsillar B cells were treated with anti-IgM or anti-CDS antibodies, capping examined after Ih (by fluorescence microscopy) and modulation after 24 h (by flow cytometry). CD5 co-capped and co-modulated with sIgM. Of various drugs tested, only the protein tyrosine kinase inhibitor (genistein) had any effect on capping and co-capping. Capping of sIgM (and co-capping of CD5) but not capping of CD5 (or co-capping of sIgM) was inhibited by genistein. None of the other drugs affecting PKC or cytoskeletal structures (colchicine and cytochalasin D) had any effect. However, the PKC inhibitors, staurosporine and H-7, inhibited the modulation of slgM by anti-IgM but not CD5 by anti-CDS. In contrast, PKC activators, PMA and mezerein, inhibited modulation of CD5 by anti-CDS but not sIgM by anti-IgM. This suggests that direct ligation of CD5 utilizes different signalling pathways compared with sIgM. It seems likely that in CD5+ B cells, interaction of CD5 with its ligand CD72 modulates signals transmitted through the BcR.