Involvement of CD5 in T_h1 and T_h2 contactmediated rescue of anti-μ and ionomycin induced growth inhibition in a B cell lymphoma

Cross-linking of membrane Ig receptors by anti-i 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-μ and ionomycin were overcome by anti-CD3-activated T_h2 clones D10.G4 and F1 and by T_h1 cell clone S53. In this report the T_h-mediated growth reversal in BKS-2 cells was shown to require contact-dependent interactions when the inhibition was caused by immobilized anti-μ or ionomycin. T_h2 cells in transwells (lymphokines) failed to protect BKS-2 cells from the growth-inhibitory effect of immobilized anti-μ or Ionomycin. Monoclonal antibodies to CD5 or CD40 llgands on activated T_h cells partially inhibited the T_h2 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 T_h cell mediated growth reversal of BKS-2 cells. These data demonstrated that noncognate physical interaction with T_h cells was essential for the recovery of BKS-2 cells when the latter were growth-arrested by strong inhibitory stimull such as immobilized anti-μ and ionomycin. Further CD5 as well as CD40 llgands on T_h cells are important for signal transductlon in this type of T-B interaction.