MHC-SPECIFIC RECOGNITION OF A BACTERIAL SUPERANTIGEN BY WEAKLY REACTIVE T-CELLS

Previous studies have suggested that MHC class II polymorphism can inf luence the recognition of retroviral superantigen by murine T cells th at have an intrinsically weak avidity for the superantigen. The aim of the present study was to determine whether bacterial superantigen rec ognition also is influenced by MHC polymorphism. Therefore, we screene d for TCR with a low avidity for the bacterial superantigen SEB, and i dentified two V beta elements (V beta 14 and V beta 16) that had not b een associated previously with SEB recognition. This finding extends t he number of previously identified SEB-reactive V beta elements (V bet a 6, V beta 7, V beta 8.1, V beta 8.2, and V beta 8.3) to at least sev en. A detailed comparison of SEB recognition by V beta 14(+) and V bet a 8.2(+) T cell hybridomas revealed two interesting features. First, S EB recognition by V beta 14(+) hybridomas was relatively weak compared with V beta 8.2(+) hybridomas. Second, in contrast to V beta 8.2(+) h ybridomas, individual V beta 14(+) hybridomas responded differentially to SEB presented by either I-E(d) or I-E(k) molecules on the surface of L cell transfectants, indicating a role for polymorphic residues of the MHC in superantigen presentation. These findings demonstrate that T cell recognition of bacterial superantigens can be influenced by MH C polymorphism in a manner analogous to that of retroviral superantige n recognition, and that this characteristic is a feature of low avidit y T cells. Taken together, these data support the hypothesis that ther e is a direct interaction between the TCR and MHC molecules during sup erantigen recognition.