MICAA4 protects against ulcerative colitis, whereas MICAA5.1 is associated with abscess formation and age of onset
Summary Ulcerative colitis (UC) is one of the two major forms of inflammatory bowel disease, the aetiology of which remains unknown. Several studies have demonstrated the genetic basis of disease, identifying more than 130 susceptibility loci. The major histocompatibility complex class I chain‐relat...
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| Veröffentlicht in: | Clinical and experimental immunology 2016-06, Vol.184 (3), p.323-331 |
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| creator | Martinez‐Chamorro, A. Moreno, A. Gómez‐García, M. Cabello, M. J. Martin, J. Lopez‐Nevot, M. Á. |
| description | Summary
Ulcerative colitis (UC) is one of the two major forms of inflammatory bowel disease, the aetiology of which remains unknown. Several studies have demonstrated the genetic basis of disease, identifying more than 130 susceptibility loci. The major histocompatibility complex class I chain‐related gene A (MICA) is a useful candidate to be involved in UC pathogenesis, because it could be important in recognizing the integrity of the epithelial cell and its response to stress. The aim of this study was to analyse the relationship between polymorphisms in the transmembrane domain of MICA and susceptibility to develop UC. A total of 340 patients with UC and 636 healthy controls were genotyped for MICA transmembrane polymorphism using a polymerase chain reaction (PCR) combined with fluorescent technology. Different MICA alleles were determined depending on the PCR product size. The allele MICA*A4 was less frequent in patients than in controls (P = 0·003; OR = 0·643), and this protective role is higher when it forms haplotype with B*27 (P = 0·002; OR = 0·294). The haplotype HLA‐B*52/MICA*A6 was also associated with UC [P = 0·001; odds ratio (OR) = 2·914]. No other alleles, genotypes or haplotypes were related with UC risk. Moreover, MICA*A5.1 is associated independently with abscesses (P = 0·002; OR = 3·096) and its frequency is lower in patients diagnosed between ages 17 and 40 years (P = 0·007; OR = 0·633), meaning an extreme age on onset. No association with location, extra‐intestinal manifestations or need for surgery was found. |
| doi_str_mv | 10.1111/cei.12786 |
| format | Article |
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Ulcerative colitis (UC) is one of the two major forms of inflammatory bowel disease, the aetiology of which remains unknown. Several studies have demonstrated the genetic basis of disease, identifying more than 130 susceptibility loci. The major histocompatibility complex class I chain‐related gene A (MICA) is a useful candidate to be involved in UC pathogenesis, because it could be important in recognizing the integrity of the epithelial cell and its response to stress. The aim of this study was to analyse the relationship between polymorphisms in the transmembrane domain of MICA and susceptibility to develop UC. A total of 340 patients with UC and 636 healthy controls were genotyped for MICA transmembrane polymorphism using a polymerase chain reaction (PCR) combined with fluorescent technology. Different MICA alleles were determined depending on the PCR product size. The allele MICA*A4 was less frequent in patients than in controls (P = 0·003; OR = 0·643), and this protective role is higher when it forms haplotype with B*27 (P = 0·002; OR = 0·294). The haplotype HLA‐B*52/MICA*A6 was also associated with UC [P = 0·001; odds ratio (OR) = 2·914]. No other alleles, genotypes or haplotypes were related with UC risk. Moreover, MICA*A5.1 is associated independently with abscesses (P = 0·002; OR = 3·096) and its frequency is lower in patients diagnosed between ages 17 and 40 years (P = 0·007; OR = 0·633), meaning an extreme age on onset. No association with location, extra‐intestinal manifestations or need for surgery was found.</description><identifier>ISSN: 0009-9104</identifier><identifier>EISSN: 1365-2249</identifier><identifier>DOI: 10.1111/cei.12786</identifier><identifier>PMID: 26940143</identifier><language>eng</language><publisher>England: Oxford University Press</publisher><subject>Abscess - diagnosis ; Abscess - genetics ; Abscess - immunology ; Abscess - pathology ; Adult ; Age of Onset ; Alleles ; Amino Acid Sequence ; autoimmunity ; Case-Control Studies ; cell surface molecules ; Colitis, Ulcerative - diagnosis ; Colitis, Ulcerative - genetics ; Colitis, Ulcerative - immunology ; Colitis, Ulcerative - pathology ; Female ; Gene Expression ; Gene Frequency ; Genetic Predisposition to Disease ; Haplotypes ; Histocompatibility Antigens Class I - genetics ; Histocompatibility Antigens Class I - immunology ; HLA-B27 Antigen - genetics ; HLA-B27 Antigen - immunology ; HLA-B52 Antigen - genetics ; HLA-B52 Antigen - immunology ; Humans ; inflammation ; Male ; MHC ; Middle Aged ; Models, Molecular ; molecular biology ; Odds Ratio ; Original ; Polymorphism, Genetic - immunology ; Protein Domains ; Protein Isoforms - genetics ; Protein Isoforms - immunology ; Sequence Alignment</subject><ispartof>Clinical and experimental immunology, 2016-06, Vol.184 (3), p.323-331</ispartof><rights>2016 British Society for Immunology</rights><rights>2016 British Society for Immunology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4766-ffdd744ecb0e8d2eeec2a25c993710a25f3bf6185f1a1eb7da19fbdb0384f3b43</citedby><cites>FETCH-LOGICAL-c4766-ffdd744ecb0e8d2eeec2a25c993710a25f3bf6185f1a1eb7da19fbdb0384f3b43</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872378/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4872378/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26940143$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Martinez‐Chamorro, A.</creatorcontrib><creatorcontrib>Moreno, A.</creatorcontrib><creatorcontrib>Gómez‐García, M.</creatorcontrib><creatorcontrib>Cabello, M. J.</creatorcontrib><creatorcontrib>Martin, J.</creatorcontrib><creatorcontrib>Lopez‐Nevot, M. Á.</creatorcontrib><title>MICAA4 protects against ulcerative colitis, whereas MICAA5.1 is associated with abscess formation and age of onset</title><title>Clinical and experimental immunology</title><addtitle>Clin Exp Immunol</addtitle><description>Summary
Ulcerative colitis (UC) is one of the two major forms of inflammatory bowel disease, the aetiology of which remains unknown. Several studies have demonstrated the genetic basis of disease, identifying more than 130 susceptibility loci. The major histocompatibility complex class I chain‐related gene A (MICA) is a useful candidate to be involved in UC pathogenesis, because it could be important in recognizing the integrity of the epithelial cell and its response to stress. The aim of this study was to analyse the relationship between polymorphisms in the transmembrane domain of MICA and susceptibility to develop UC. A total of 340 patients with UC and 636 healthy controls were genotyped for MICA transmembrane polymorphism using a polymerase chain reaction (PCR) combined with fluorescent technology. Different MICA alleles were determined depending on the PCR product size. The allele MICA*A4 was less frequent in patients than in controls (P = 0·003; OR = 0·643), and this protective role is higher when it forms haplotype with B*27 (P = 0·002; OR = 0·294). The haplotype HLA‐B*52/MICA*A6 was also associated with UC [P = 0·001; odds ratio (OR) = 2·914]. No other alleles, genotypes or haplotypes were related with UC risk. Moreover, MICA*A5.1 is associated independently with abscesses (P = 0·002; OR = 3·096) and its frequency is lower in patients diagnosed between ages 17 and 40 years (P = 0·007; OR = 0·633), meaning an extreme age on onset. No association with location, extra‐intestinal manifestations or need for surgery was found.</description><subject>Abscess - diagnosis</subject><subject>Abscess - genetics</subject><subject>Abscess - immunology</subject><subject>Abscess - pathology</subject><subject>Adult</subject><subject>Age of Onset</subject><subject>Alleles</subject><subject>Amino Acid Sequence</subject><subject>autoimmunity</subject><subject>Case-Control Studies</subject><subject>cell surface molecules</subject><subject>Colitis, Ulcerative - diagnosis</subject><subject>Colitis, Ulcerative - genetics</subject><subject>Colitis, Ulcerative - immunology</subject><subject>Colitis, Ulcerative - pathology</subject><subject>Female</subject><subject>Gene Expression</subject><subject>Gene Frequency</subject><subject>Genetic Predisposition to Disease</subject><subject>Haplotypes</subject><subject>Histocompatibility Antigens Class I - genetics</subject><subject>Histocompatibility Antigens Class I - immunology</subject><subject>HLA-B27 Antigen - genetics</subject><subject>HLA-B27 Antigen - immunology</subject><subject>HLA-B52 Antigen - genetics</subject><subject>HLA-B52 Antigen - immunology</subject><subject>Humans</subject><subject>inflammation</subject><subject>Male</subject><subject>MHC</subject><subject>Middle Aged</subject><subject>Models, Molecular</subject><subject>molecular biology</subject><subject>Odds Ratio</subject><subject>Original</subject><subject>Polymorphism, Genetic - immunology</subject><subject>Protein Domains</subject><subject>Protein Isoforms - genetics</subject><subject>Protein Isoforms - immunology</subject><subject>Sequence Alignment</subject><issn>0009-9104</issn><issn>1365-2249</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkV1rFDEUhoNY7Fq98A9IwBsFZ5tkMvm4EcrS1kJLb_Q6ZDIn3ZTZyZpkuvTfG7u1qCDNTRLOk4ec8yL0jpIlrevYQVhSJpV4gRa0FV3DGNcv0YIQohtNCT9Er3O-rVchBHuFDpnQnFDeLlC6ulidnHC8TbGAKxnbGxumXPA8Oki2hDvALo6hhPwZ79aQwGb88KZbUhwqn3N0wRYY8C6UNbZ9dpAz9jFt6vM4YTsN1Qo4ehynDOUNOvB2zPD2cT9C389Ov62-NpfX51V82TguhWi8HwbJObiegBoYADhmWee0biUl9eTb3guqOk8thV4OlmrfDz1pFa8l3h6hL3vvdu43MDiYSrKj2aawseneRBvM35UprM1NvDNcSdZKVQUfHwUp_pghF7MJtblxtBPEORuqiBK8jlQ8j0pNeMcEkxX98A96G-c01UlUSmlJRUu7Sn3aUy7FnBP4p39TYn6Fbmro5iH0yr7_s9En8nfKFTjeA7swwv3_TWZ1erFX_gTtP7a7</recordid><startdate>201606</startdate><enddate>201606</enddate><creator>Martinez‐Chamorro, A.</creator><creator>Moreno, A.</creator><creator>Gómez‐García, M.</creator><creator>Cabello, M. J.</creator><creator>Martin, J.</creator><creator>Lopez‐Nevot, M. Á.</creator><general>Oxford University Press</general><general>John Wiley and Sons Inc</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>7U9</scope><scope>H94</scope><scope>M7N</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>201606</creationdate><title>MICAA4 protects against ulcerative colitis, whereas MICAA5.1 is associated with abscess formation and age of onset</title><author>Martinez‐Chamorro, A. ; Moreno, A. ; Gómez‐García, M. ; Cabello, M. J. ; Martin, J. ; Lopez‐Nevot, M. Á.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4766-ffdd744ecb0e8d2eeec2a25c993710a25f3bf6185f1a1eb7da19fbdb0384f3b43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Abscess - diagnosis</topic><topic>Abscess - genetics</topic><topic>Abscess - immunology</topic><topic>Abscess - pathology</topic><topic>Adult</topic><topic>Age of Onset</topic><topic>Alleles</topic><topic>Amino Acid Sequence</topic><topic>autoimmunity</topic><topic>Case-Control Studies</topic><topic>cell surface molecules</topic><topic>Colitis, Ulcerative - diagnosis</topic><topic>Colitis, Ulcerative - genetics</topic><topic>Colitis, Ulcerative - immunology</topic><topic>Colitis, Ulcerative - pathology</topic><topic>Female</topic><topic>Gene Expression</topic><topic>Gene Frequency</topic><topic>Genetic Predisposition to Disease</topic><topic>Haplotypes</topic><topic>Histocompatibility Antigens Class I - genetics</topic><topic>Histocompatibility Antigens Class I - immunology</topic><topic>HLA-B27 Antigen - genetics</topic><topic>HLA-B27 Antigen - immunology</topic><topic>HLA-B52 Antigen - genetics</topic><topic>HLA-B52 Antigen - immunology</topic><topic>Humans</topic><topic>inflammation</topic><topic>Male</topic><topic>MHC</topic><topic>Middle Aged</topic><topic>Models, Molecular</topic><topic>molecular biology</topic><topic>Odds Ratio</topic><topic>Original</topic><topic>Polymorphism, Genetic - immunology</topic><topic>Protein Domains</topic><topic>Protein Isoforms - genetics</topic><topic>Protein Isoforms - immunology</topic><topic>Sequence Alignment</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Martinez‐Chamorro, A.</creatorcontrib><creatorcontrib>Moreno, A.</creatorcontrib><creatorcontrib>Gómez‐García, M.</creatorcontrib><creatorcontrib>Cabello, M. J.</creatorcontrib><creatorcontrib>Martin, J.</creatorcontrib><creatorcontrib>Lopez‐Nevot, M. Á.</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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Clinical and experimental immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Martinez‐Chamorro, A.</au><au>Moreno, A.</au><au>Gómez‐García, M.</au><au>Cabello, M. J.</au><au>Martin, J.</au><au>Lopez‐Nevot, M. Á.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MICAA4 protects against ulcerative colitis, whereas MICAA5.1 is associated with abscess formation and age of onset</atitle><jtitle>Clinical and experimental immunology</jtitle><addtitle>Clin Exp Immunol</addtitle><date>2016-06</date><risdate>2016</risdate><volume>184</volume><issue>3</issue><spage>323</spage><epage>331</epage><pages>323-331</pages><issn>0009-9104</issn><eissn>1365-2249</eissn><abstract>Summary
Ulcerative colitis (UC) is one of the two major forms of inflammatory bowel disease, the aetiology of which remains unknown. Several studies have demonstrated the genetic basis of disease, identifying more than 130 susceptibility loci. The major histocompatibility complex class I chain‐related gene A (MICA) is a useful candidate to be involved in UC pathogenesis, because it could be important in recognizing the integrity of the epithelial cell and its response to stress. The aim of this study was to analyse the relationship between polymorphisms in the transmembrane domain of MICA and susceptibility to develop UC. A total of 340 patients with UC and 636 healthy controls were genotyped for MICA transmembrane polymorphism using a polymerase chain reaction (PCR) combined with fluorescent technology. Different MICA alleles were determined depending on the PCR product size. The allele MICA*A4 was less frequent in patients than in controls (P = 0·003; OR = 0·643), and this protective role is higher when it forms haplotype with B*27 (P = 0·002; OR = 0·294). The haplotype HLA‐B*52/MICA*A6 was also associated with UC [P = 0·001; odds ratio (OR) = 2·914]. No other alleles, genotypes or haplotypes were related with UC risk. Moreover, MICA*A5.1 is associated independently with abscesses (P = 0·002; OR = 3·096) and its frequency is lower in patients diagnosed between ages 17 and 40 years (P = 0·007; OR = 0·633), meaning an extreme age on onset. No association with location, extra‐intestinal manifestations or need for surgery was found.</abstract><cop>England</cop><pub>Oxford University Press</pub><pmid>26940143</pmid><doi>10.1111/cei.12786</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Abscess - diagnosis Abscess - genetics Abscess - immunology Abscess - pathology Adult Age of Onset Alleles Amino Acid Sequence autoimmunity Case-Control Studies cell surface molecules Colitis, Ulcerative - diagnosis Colitis, Ulcerative - genetics Colitis, Ulcerative - immunology Colitis, Ulcerative - pathology Female Gene Expression Gene Frequency Genetic Predisposition to Disease Haplotypes Histocompatibility Antigens Class I - genetics Histocompatibility Antigens Class I - immunology HLA-B27 Antigen - genetics HLA-B27 Antigen - immunology HLA-B52 Antigen - genetics HLA-B52 Antigen - immunology Humans inflammation Male MHC Middle Aged Models, Molecular molecular biology Odds Ratio Original Polymorphism, Genetic - immunology Protein Domains Protein Isoforms - genetics Protein Isoforms - immunology Sequence Alignment |
| title | MICAA4 protects against ulcerative colitis, whereas MICAA5.1 is associated with abscess formation and age of onset |
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