Analysis of Mlsc genetics. A novel instance of genetic redundancy

J Exp Med. 1989 Oct 1;170(4):1059-73. doi: 10.1084/jem.170.4.1059.

Abstract

The identity of the self determinants involved in the selection of the T cell repertoire has been a matter of considerable interest. In addition to the apparent critical role of MHC gene products, accumulated experimental results indicate the importance of non-MHC gene products in T cell repertoire selection. In particular, murine Mlsa and Mlsc determinants have been shown to be highly stimulatory to allogeneic T cells and to be involved in the negative selection (elimination) of self-reactive T cells expressing selected TCR V beta segments. In this work, a unique phenomenon of genetic redundancy is described in the control of Mlsc expression: Mlsc appears to be controlled by at least two unlinked loci, and the product of either one of these loci is sufficient to evoke Mlsc-specific T cell response and to act as a ligand in the deletion of self Mlsc-reactive V beta 3+ T cells. Based on these findings, we propose a possible explanation for the fact that Mls-like genes or gene products have not been identified in other species such as man.

MeSH terms

  • Animals
  • Antigens, Surface / genetics*
  • Epitopes
  • Genes
  • Genetic Linkage
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred Strains / genetics
  • Mice, Inbred Strains / immunology
  • Minor Histocompatibility Loci*
  • Minor Lymphocyte Stimulatory Antigens
  • Receptors, Antigen, T-Cell / genetics
  • Receptors, Antigen, T-Cell, alpha-beta
  • Spleen / immunology
  • T-Lymphocytes / immunology*

Substances

  • Antigens, Surface
  • Epitopes
  • Minor Lymphocyte Stimulatory Antigens
  • Receptors, Antigen, T-Cell
  • Receptors, Antigen, T-Cell, alpha-beta