Positive signal transduction via surface CD4 molecules does not need coexpression of the CD3/TcR complex

We previously reported that the human CD4 molecule is capable of transducing a positive signal when activated by an anti-CD4 mAb B66. This antibody, in contrast to many other anti-CD4 mAb, induced IL2 production and proliferation of resting CD4 + peripheral blood T lymphocytes in the absence of any other signal. We further reported that anti-CD4 mAb B66 was able to induce IL2 production in murine T-cell hybridoma cells transfected with full-length human CD4 cDNA. In the present study, we extend these findings by demonstrating that anti-CD4 mAb B66 was able to induce Ca 2+ mobilization and IL2 production in a CD3/TcR- variant 31-13, of the CD3/TcR + Jurkat cell line. We further showed that anti-CD4 mAb B66 was able to activate CD4 + mobilization when cross-linked with a second antibody and, in addition, the production of large quantities of IL1β was measured. In essence, our findings provide direct evidence that cross-linking of CD4 may cause T-cell activation in the absence of the coexpression of the CD3/TcR molecular complex and that, in addition, CD4 might transduce a positive signal in CD4 + cells of the myeloid lineage.