Critical role of endogenous Mtv in acute lethal graft-versus-host disease.
Little is known about the etiology of the graft-versus-host disease (GVHD) occuring after transplantation of lymphoid cells incompatible for minor histocompatibility antigens (mHAg). Here, the potential role of host endogenous mouse mammary tumor virus (Mtv)-encoded superantigens (SAg) in the development of lethal GVHD was investigated. In a combination of H-2d compatible mice, the presence of Mtv-7 and, to a lesser extent, of Mtv-1, -6, -13 in the host genome, highly increases the rate and severity of GVHD. Kinetic analyses of TCR V beta gene expression in recipient mice consistently indicate a dramatic but transient infiltration of GVHD target organs by Mtv-SAg-specific T cells. This suggests that SAg encoded by endogenous Mtv, by activating large T cell subpopulations, would help the response to mHAg and thus play a critical role in the initiation or aggravation of GVHD.
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INSERM, U267, Hopital Paul Brousse, Villejuif, France.
Roger
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Seman
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Bruley-Rosset
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D000208:Acute Disease; D000818:Animals; D006086:Graft vs Host Disease / Q000209:etiology* / Q000401:mortality; D008324:Mammary Tumor Virus, Mouse / Q000276:immunology / Q000502:physiology*; D051379:Mice; D008815:Mice, Inbred Strains; D011533:Proviruses / Q000502:physiology*; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000032:analysis; D018089:Superantigens / Q000502:physiology*; D013601:T-Lymphocytes / Q000276:immunology
D016693:Receptors, Antigen, T-Cell, alpha-beta; D018089:Superantigens