The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3

Marie Claude Morse, Gilles Bleau, Vikram M. Dabhi, Francis Hétu, Elliot A. Drobetsky, Kirsten Fischer Lindahl, Claude Perreault

Research output: Contribution to journalArticlepeer-review

54 Scopus citations

Abstract

We found that (LP x C57BL/6)F1 mice could raise a CTL response against parental C57BL/6 cells. These CTLs recognized a maternally transmitted, H2- M3(w1)-restricted, minor histocompatibility Ag (MiHA) that is widely distributed among many strains of mice and encoded by the COI mitochondrial gene. The wild-type MiHA is the COI N-terminal hexapeptide. Sequencing the 5' end of the COI gene in LP and C57BL/6 mice showed that the LP allele arose by a T→C transition in the third codon, which caused substitution of threonine for isoleucine. Molecular characterization of this MiHA and the demonstration that it is presented exclusively by H2-M3: 1) support the concept that differential expression of MiHA in MHC-identical animals is caused by polymorphism of the MiHA gene proper; 2) expand our knowledge of the repertoire of self-peptides naturally presented by H2-M3 and show that this MHC class I molecule can present short endogenous peptide ligands; and 3) suggest that mitochondrial DNA mutations that modify the repertoire of H2- M3-associated mitochondrial peptides are representative of mitochondrial DNA mutations in general.

Original languageEnglish (US)
Pages (from-to)3301-3307
Number of pages7
JournalJournal of Immunology
Volume156
Issue number9
StatePublished - May 1 1996

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology

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