LP-BM5 murine retrovirus-induced immunodeficiency disease in allogeneic SCID chimeric mice. Inability to recognize a putative viral superantigen does not prevent induction of disease.
T cell recognition of viral superantigens has been postulated to contribute to the pathogenesis of the immunodeficiency disease induced in mice by infection with the LP-BM5 murine leukemia virus complex. A candidate superantigen has been identified in the B cell lymphoma line B6-1710 derived from an LP-BM5-infected C57BL/6 (H-2b) mouse. We have asked whether the stimulatory activity expressed by B6-1710 behaves as a superantigen by assessing the ability of T cells from fully allogeneic H-2b-->H-2d SCID chimeric mice to respond to the line. T cells from allochimeric mice failed to respond to B6-1710, whereas they responded normally to Staphylococcus enterotoxin B, a well characterized superantigen. Despite this finding, allochimeric mice were fully susceptible to the immune deficiency disease induced by LP-BM5 virus infection. These findings show that the role of superantigen expression in retrovirus-induced immune deficiency disease remains to be defined.
Division of Immunology, Medical Biology Institute, La Jolla, California 92037.
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Gilmore
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Cowing
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Mosier
D000818:Animals; D000956:Antigens, Viral / Q000276:immunology* / Q000502:physiology; D002678:Chimera; D006183:H-2 Antigens / Q000235:genetics / Q000276:immunology; D009052:Leukemia Virus, Murine / Q000276:immunology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D016513:Mice, SCID / Q000235:genetics; D016511:Severe Combined Immunodeficiency / Q000209:etiology* / Q000235:genetics / Q000517:prevention & control; D013601:T-Lymphocytes / Q000502:physiology
D000956:Antigens, Viral; D006183:H-2 Antigens