Involvement of CD5 in Th1 and Th2 contact-mediated rescue of anti-mu and ionomycin induced growth inhibition in a B cell lymphoma.

Cross-linking of membrane Ig receptors by anti-mu antibodies (Ab) or treatment with ionomycin induced complete growth arrest and subsequent apoptotic cell death in an immature B cell lymphoma, BKS-2. The growth-inhibitory signals delivered by anti-mu and ionomycin were overcome by anti-CD3-activated Th2 clones D10.G4 and F1 and by Th1 cell clone S53. In this report the Th-mediated growth reversal in BKS-2 cells was shown to require contact-dependent interactions when the inhibition was caused by immobilized anti-mu or ionomycin. Th2 cells in transwells (lymphokines) failed to protect BKS-2 cells from the growth-inhibitory effect of immobilized anti-mu or ionomycin. Monoclonal antibodies to CD5 or CD40 ligands on activated Th cells partially inhibited the Th2 contact-dependent growth reversal of BKS-2 cells whereas simultaneous addition of both antibodies effectively prevented the delivery of contact-mediated growth signal. In contrast, anti-class I or class II Ab did not affect Th cell mediated growth reversal of BKS-2 cells. These data demonstrated that noncognate physical interaction with Th cells was essential for the recovery of BKS-2 cells when the latter were growth-arrested by strong inhibitory stimuli such as immobilized anti-mu and ionomycin. Further CD5 as well as CD40 ligands on Th cells are important for signal transduction in this type of T-B interaction.