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.
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M3 - Article
C2 - 8617953
AN - SCOPUS:0029885749
SN - 0022-1767
VL - 156
SP - 3301
EP - 3307
JO - Journal of Immunology
JF - Journal of Immunology
IS - 9
ER -