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 journalArticle

54 Citations (Scopus)

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

Fingerprint

Minor Histocompatibility Antigens
Histocompatibility
Mitochondrial Genes
Mitochondrial DNA
Peptides
Mutation
Isoleucine
Threonine
Inbred C57BL Mouse
Codon
Genes
Alleles
Ligands

ASJC Scopus subject areas

  • Immunology

Cite this

Morse, M. C., Bleau, G., Dabhi, V. M., Hétu, F., Drobetsky, E. A., Lindahl, K. F., & Perreault, C. (1996). The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3. Journal of Immunology, 156(9), 3301-3307.

The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3. / Morse, Marie Claude; Bleau, Gilles; Dabhi, Vikram M.; Hétu, Francis; Drobetsky, Elliot A.; Lindahl, Kirsten Fischer; Perreault, Claude.

In: Journal of Immunology, Vol. 156, No. 9, 01.05.1996, p. 3301-3307.

Research output: Contribution to journalArticle

Morse, MC, Bleau, G, Dabhi, VM, Hétu, F, Drobetsky, EA, Lindahl, KF & Perreault, C 1996, 'The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3', Journal of Immunology, vol. 156, no. 9, pp. 3301-3307.
Morse MC, Bleau G, Dabhi VM, Hétu F, Drobetsky EA, Lindahl KF et al. The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3. Journal of Immunology. 1996 May 1;156(9):3301-3307.
Morse, Marie Claude ; Bleau, Gilles ; Dabhi, Vikram M. ; Hétu, Francis ; Drobetsky, Elliot A. ; Lindahl, Kirsten Fischer ; Perreault, Claude. / The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3. In: Journal of Immunology. 1996 ; Vol. 156, No. 9. pp. 3301-3307.
@article{951e097422184bfbb23d7de73c45a74e,
title = "The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3",
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.",
author = "Morse, {Marie Claude} and Gilles Bleau and Dabhi, {Vikram M.} and Francis H{\'e}tu and Drobetsky, {Elliot A.} and Lindahl, {Kirsten Fischer} and Claude Perreault",
year = "1996",
month = "5",
day = "1",
language = "English (US)",
volume = "156",
pages = "3301--3307",
journal = "Journal of Immunology",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "9",

}

TY - JOUR

T1 - The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3

AU - Morse, Marie Claude

AU - Bleau, Gilles

AU - Dabhi, Vikram M.

AU - Hétu, Francis

AU - Drobetsky, Elliot A.

AU - Lindahl, Kirsten Fischer

AU - Perreault, Claude

PY - 1996/5/1

Y1 - 1996/5/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0029885749&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0029885749&partnerID=8YFLogxK

M3 - Article

C2 - 8617953

AN - SCOPUS:0029885749

VL - 156

SP - 3301

EP - 3307

JO - Journal of Immunology

JF - Journal of Immunology

SN - 0022-1767

IS - 9

ER -