CD5+B Cells: Differential Capping and Modulation of IgM and CD5

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Abstract
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 withanti‐IgM or anti‐CD5 antibodies, capping examined after 1 h (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 kinaseinhibitor (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 sIgM by anti‐IgM but not CD5 by anti‐CD5. In contrast, PKC activators, PMA and mezerein, inhibited modulation of CD5 by anti‐CD5 but notsIgM 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 theBcR.

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