Abstract
L1-16, a DR-specific, nonpolymorphic monoclonal antibody (MoAb) recognizing the beta-chain of the molecule, blocked virus-specific as well as allogeneic-proliferative T cell responses, whereas another nonpolymorphic anti-DR MoAb blocked proliferative responses to allogeneic cells only. IL 2-supernatants reversed the blocking induced by L1-16. On the other hand class I-specific MoAb B1-23-2 (HLA-A-B-C-specific) and M 18 (beta 2 microglobulin-specific) and their F(ab')2 fragments blocked equally virus-specific or allogeneic proliferative responses. IL 2-containing supernatants did not reverse this phenomenon. Neither anti-class I nor anti-class II MoAb inhibited the IL 2-induced proliferation of IL 2-dependent established T cell lines. MoAb acted neither at the antigen-presenting cell level nor by a toxic effect nor by inducing suppressor cells. These results suggest that a) different epitopes of the DR molecule can be involved during responses to influenza viruses and allogeneic antigens; b) the epitope recognized by L1-16 on the beta-chain of the DR molecule seem necessary for IL 2 production by lymphocytes after activation with influenza antigens; and c) class I-specific MoAb block DR-restricted proliferative responses of lymphocytes by an as yet unknown mechanism.
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