RESUMO
MAb anti-Leu-13 reacts with a 16-kDa-interferon-responsive lymphocyte-endothelial cell surface antigen and has been demonstrated to induce lymphocyte aggregation by an undefined adhesion pathway. While anti-Leu-13 inhibits proliferation triggered by CD3 antibodies it was found to consistently augment proliferation induced by a pair of CD2 antibodies at suboptimally mitogenic concentrations. The latter mechanism of T cell activation may represent an antigen-nonspecific activation pathway requiring extensive cell-cell interaction. Proliferation induced via the CD2 pathway was very sensitive to the presence of monocytes whose inhibitory effect was reversed by indomethacin. While the potent inhibitory effect of PGE2 on proliferation induced via the CD2 pathway was weakly antagonized by anti-Leu-13, the combined effects of anti-Leu-13 and PGE2 on the CD3 pathway were additive and very inhibitory. The possibility that the Leu-13 signal reflects a mechanism by which a monocyte/macrophage-sensitive T cell activation pathway might be selectively amplified in vivo is discussed.