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The Journal of Immunology, Vol 150, Issue 4 1422-1428, Copyright © 1993 by American Association of Immunologists

ARTICLES

Association of a V beta 2-specific superantigen with a tumorigenic milk- borne mouse mammary tumor virus

RJ Hodes, MB Novick, LD Palmer and JE Knepper
Experimental Immunology Branch, National Cancer Institute, National Institutes of Health, Bethesda, MD 20892.

A number of endogenous mouse mammary tumor virus (MMTV) proviruses encode superantigens that have the property of stimulating mature T lymphocytes in a TCR V beta-specific fashion and of mediating V beta- specific clonal deletion in developing T cells. The tumorigenic milk- borne MMTV carried by C3H and GR mice also have superantigen properties in vivo, and it has been proposed that this superantigenic function is critical to the infectivity and/or tumorigenicity of the virus. To test the requirement for superantigen properties in tumorigenic MMTV, a highly tumorigenic strain of MMTV isolated from BALB/c mice (BALB/cV virus) was analyzed for its effect on TCR V beta expression. It was found that exposure of newborn mice to milk-borne virus results in marked deletion of V beta 2-expressing CD4+ peripheral T cells. This deletion is detected in mature TCRhigh thymocytes as well as in peripheral T cells from virus-exposed mice. Deletion is dependent on expression of a permissive MHC type in mice exposed to virus. Subcutaneous injection of adult mice with virus-containing milk induces a substantial increase in V beta 2+ CD4+ cells in draining lymph nodes within 4 days. Thus, tumorigenic BALB/cV is associated with V beta 2- specific superantigen activity capable of mediating both T cell expansion and clonal deletion in vivo. These findings are consistent with a critical role of superantigen-mediated T cell activation in MMTV infection and tumorigenesis.


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