The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3
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-M3wt-restricted, minor histocompatibility Ag (MiHA) that is widely distributed among many strains of mice and encoded by the COI mitochondrial gene. The w...
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Veröffentlicht in: | The Journal of immunology (1950) 1996-05, Vol.156 (9), p.3301-3307 |
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creator | Morse, MC Bleau, G Dabhi, VM Hetu, F Drobetsky, EA Lindahl, KF Perreault, C |
description | 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-M3wt-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. |
doi_str_mv | 10.4049/jimmunol.156.9.3301 |
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These CTLs recognized a maternally transmitted, H2-M3wt-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.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.156.9.3301</identifier><identifier>PMID: 8617953</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Amino Acid Sequence ; Animals ; Antigen Presentation - genetics ; Base Sequence ; Crosses, Genetic ; DNA, Mitochondrial - immunology ; Electron Transport Complex IV - genetics ; Electron Transport Complex IV - immunology ; Female ; H-2 Antigens - immunology ; Male ; Maternal-Fetal Exchange - immunology ; Mice ; Mice, Inbred A ; Mice, Inbred BALB C ; Mice, Inbred C3H ; Mice, Inbred C57BL ; Mice, Inbred CBA ; Mice, Inbred NZB ; Minor Histocompatibility Antigens - chemistry ; Minor Histocompatibility Antigens - genetics ; Minor Histocompatibility Antigens - immunology ; Molecular Sequence Data ; Pregnancy ; Structure-Activity Relationship</subject><ispartof>The Journal of immunology (1950), 1996-05, Vol.156 (9), p.3301-3307</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-fb03a840e8505ff4f8fda44d7d58d9664912691c366cc2c6df661120526711e13</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8617953$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Morse, MC</creatorcontrib><creatorcontrib>Bleau, G</creatorcontrib><creatorcontrib>Dabhi, VM</creatorcontrib><creatorcontrib>Hetu, F</creatorcontrib><creatorcontrib>Drobetsky, EA</creatorcontrib><creatorcontrib>Lindahl, KF</creatorcontrib><creatorcontrib>Perreault, C</creatorcontrib><title>The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>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-M3wt-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.</description><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Antigen Presentation - genetics</subject><subject>Base Sequence</subject><subject>Crosses, Genetic</subject><subject>DNA, Mitochondrial - immunology</subject><subject>Electron Transport Complex IV - genetics</subject><subject>Electron Transport Complex IV - immunology</subject><subject>Female</subject><subject>H-2 Antigens - immunology</subject><subject>Male</subject><subject>Maternal-Fetal Exchange - immunology</subject><subject>Mice</subject><subject>Mice, Inbred A</subject><subject>Mice, Inbred BALB C</subject><subject>Mice, Inbred C3H</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred CBA</subject><subject>Mice, Inbred NZB</subject><subject>Minor Histocompatibility Antigens - chemistry</subject><subject>Minor Histocompatibility Antigens - genetics</subject><subject>Minor Histocompatibility Antigens - immunology</subject><subject>Molecular Sequence Data</subject><subject>Pregnancy</subject><subject>Structure-Activity Relationship</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkLFu2zAURYkiReKk_YKiAKd0ksMnkY_SWBhpEyBBlhToRtDkU8RAEl1ShuG_rwy7QbZOd7jn3uEw9gXEUgrZ3LyGYdiOsV-CwmWzrCoBH9gClBIFosAzthCiLAvQqC_YZc6vQggUpTxn5zWCblS1YL-fO-Krp3s-hCm6Lo4-BdvzFxqJ0-iip8ztXI4x8S7kmYnDxk5hHfow7bkdpzCzfJMo0ziR5-s9vyuLx-oT-9jaPtPnU16xXz9un1d3xcPTz_vV94fCSS2nol2LytZSUK2EalvZ1q23UnrtVe0bRNlAiQ24CtG50qFvEQFKoUrUAATVFbs-_m5S_LOlPJkhZEd9b0eK22y0bmqJEv8LzhI11KBmsDqCLsWcE7Vmk8Jg096AMAfx5p_4w8Y05iB-Xn093W_XA_m3zcn03H879l146XYhkcmD7fuZBrPb7d49_QWbko2p</recordid><startdate>19960501</startdate><enddate>19960501</enddate><creator>Morse, MC</creator><creator>Bleau, G</creator><creator>Dabhi, VM</creator><creator>Hetu, F</creator><creator>Drobetsky, EA</creator><creator>Lindahl, KF</creator><creator>Perreault, C</creator><general>Am Assoc Immnol</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7T5</scope><scope>8FD</scope><scope>FR3</scope><scope>H94</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope></search><sort><creationdate>19960501</creationdate><title>The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3</title><author>Morse, MC ; Bleau, G ; Dabhi, VM ; Hetu, F ; Drobetsky, EA ; Lindahl, KF ; Perreault, C</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-fb03a840e8505ff4f8fda44d7d58d9664912691c366cc2c6df661120526711e13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Antigen Presentation - genetics</topic><topic>Base Sequence</topic><topic>Crosses, Genetic</topic><topic>DNA, Mitochondrial - immunology</topic><topic>Electron Transport Complex IV - genetics</topic><topic>Electron Transport Complex IV - immunology</topic><topic>Female</topic><topic>H-2 Antigens - immunology</topic><topic>Male</topic><topic>Maternal-Fetal Exchange - immunology</topic><topic>Mice</topic><topic>Mice, Inbred A</topic><topic>Mice, Inbred BALB C</topic><topic>Mice, Inbred C3H</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred CBA</topic><topic>Mice, Inbred NZB</topic><topic>Minor Histocompatibility Antigens - chemistry</topic><topic>Minor Histocompatibility Antigens - genetics</topic><topic>Minor Histocompatibility Antigens - immunology</topic><topic>Molecular Sequence Data</topic><topic>Pregnancy</topic><topic>Structure-Activity Relationship</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Morse, MC</creatorcontrib><creatorcontrib>Bleau, G</creatorcontrib><creatorcontrib>Dabhi, VM</creatorcontrib><creatorcontrib>Hetu, F</creatorcontrib><creatorcontrib>Drobetsky, EA</creatorcontrib><creatorcontrib>Lindahl, KF</creatorcontrib><creatorcontrib>Perreault, C</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Morse, MC</au><au>Bleau, G</au><au>Dabhi, VM</au><au>Hetu, F</au><au>Drobetsky, EA</au><au>Lindahl, KF</au><au>Perreault, C</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>1996-05-01</date><risdate>1996</risdate><volume>156</volume><issue>9</issue><spage>3301</spage><epage>3307</epage><pages>3301-3307</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><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-M3wt-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.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>8617953</pmid><doi>10.4049/jimmunol.156.9.3301</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Amino Acid Sequence Animals Antigen Presentation - genetics Base Sequence Crosses, Genetic DNA, Mitochondrial - immunology Electron Transport Complex IV - genetics Electron Transport Complex IV - immunology Female H-2 Antigens - immunology Male Maternal-Fetal Exchange - immunology Mice Mice, Inbred A Mice, Inbred BALB C Mice, Inbred C3H Mice, Inbred C57BL Mice, Inbred CBA Mice, Inbred NZB Minor Histocompatibility Antigens - chemistry Minor Histocompatibility Antigens - genetics Minor Histocompatibility Antigens - immunology Molecular Sequence Data Pregnancy Structure-Activity Relationship |
title | The COI mitochondrial gene encodes a minor histocompatibility antigen presented by H2-M3 |
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