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

J Immunol. 1993 Jan 1;150(1):185-9.

Abstract

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.

Publication types

  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigens, Viral / immunology*
  • Antigens, Viral / physiology
  • Chimera*
  • H-2 Antigens / genetics
  • H-2 Antigens / immunology
  • Leukemia Virus, Murine / immunology*
  • Mice
  • Mice, Inbred BALB C
  • Mice, Inbred C57BL
  • Mice, SCID / genetics
  • Severe Combined Immunodeficiency / etiology*
  • Severe Combined Immunodeficiency / genetics
  • Severe Combined Immunodeficiency / prevention & control
  • T-Lymphocytes / physiology

Substances

  • Antigens, Viral
  • H-2 Antigens