The CD5 molecule is expressed by a B cell subset. We have demonstrated that
resting B cells do not proliferate in response to CD5 ligation, whereas ce
lls preactivated with anti-IgM and IL-2 do so. Here, we specifically studie
d the effects of anti-CDS and anti-IgM on apoptosis of CD5(+) B cells. Both
ligation of CD5 or of surface IgM (slgM) resulted in apoptosis. This start
ed earlier following ligation of CD5 than with slgM, and both responses wer
e time dependent. CD5-induced apoptosis was independent of the epitope reco
gnized or the way the antibody was presented to the B cells. CD5(+) B cells
were more sensitive to IgM-induced apoptosis than CD5(-) B cells. Engageme
nt of CD5 or CD3 expressed by T cells failed to induce apoptosis. Our data
indicate differences in the function of CD5 molecules on tonsillar B cells,
compared with blood T cells and suggest that cross-linking CD5 on B cell a
ctivates specific pathways responsible for apoptosis.