CD2-DEFICIENT MICE GENERATE VIRUS-SPECIFIC CYTOTOXIC T-LYMPHOCYTES UPON INFECTION WITH LYMPHOCYTIC CHORIOMENINGITIS VIRUS

The major host response to many viral infections is the generation of virus-specific CTL. Many protein molecules on the surfaces of both CTL and target cells interact to mediate adhesion of the cells and genera te signals that lead to T cell activation and proliferation of virus-s pecific CTL that then mediate lysis of infected cells. One such protei n, CD2, has been shown to increase the binding affinity of CTL to infe cted cells, and, in addition, enhance CTL activation signals. To deter mine whether virus-specific CTL could be generated in the absence of C D2, mice lacking a functional CD2 gene were infected with lymphocytic choriomeningitis virus (LCMV), and the responses to the virus were mon itored. CD2-deficient mice infected intracerebrally with LCMV died as a consequence of CTL-mediated choriomeningitis, similar to control lit termates. Additionally, CD2-deficient mice inoculated i.p. with LCMV c leared the infection by 2 wk postinfection, as did control mice. Viral clearance in these mice was shown to be due to the generation of a vi gorous virus-specific MHC-restricted CTL response. Finally, to determi ne whether CD2 is essential for the generation of memory CTL, we exami ned the ability of CD2-deficient mice to generate memory CTL to LCMV a nd found normal memory CTL responses. Our results indicate that CD2 is not required for the generation of an LCMV-specific CTL response in v ivo, nor is CD2 required for the maintenance or activation of memory C TL.