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A virus-encoded "superantigen" in a retrovirus-induced immunodeficiency syndrome of mice
A W Hügin1, M S Vacchio, H C Morse
1Laboratory of Immunopathology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, MD 20892.
Abstract:
The development of an immunodeficiency syndrome of mice caused by a replication-defective murine leukemia virus (MuLV) is paradoxically associated with a rapid activation and proliferation of CD4+ T cells that are dependent on the presence of B cells. The responses of normal spleen cells to B cell lines that express the defective virus indicated that these lines express a cell surface determinant that shares "superantigenic" properties with some microbial antigens and Mls-like self antigens. This antigen elicited a potent proliferative response that was dependent on the presence of CD4+ T cells and was associated with selective expansion of cells bearing V beta 5. This response was markedly inhibited by a monoclonal antibody specific for the MuLV gag-encoded p30 antigen.