| http://purl.uniprot.org/citations/20232291 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/20232291 | http://www.w3.org/2000/01/rdf-schema#comment | "UnlabelledAutoimmune hepatitis (AIH), like many autoimmune diseases, is most prevalent in young women. The immunological basis of this age and sex susceptibility bias was investigated in a murine model of AIH. Xenoimmunization of 7-week-old female C57BL/6 mice resulted in more severe AIH with higher levels of liver inflammation, serum alanine aminotransferase, specific T-cell cytotoxicity, and autoantibody than younger and older females. Vaccinated males developed minimal liver inflammation and higher percentages of CD4(+)CD25(+)FoxP3(+) regulatory T cell in peripheral blood mononuclear cells, spleen, and liver than females. Regulatory T cells (Tregs) were virtually absent in liver-lymphocytes infiltrates of females. Castration of C57BL/6 mice, with or without 17beta-estradiol supplementation, did not modify susceptibility in males, nor Treg numbers, suggesting minimal contribution of testosterone and estradiol to autoimmune hepatitis (AIH) susceptibility. Xenoimmunized Aire(+/0) mouse displayed similar AIH susceptibility, sex bias, and Tregs numbers as C57BL/6 mice, suggesting that susceptibility in females is not the result of less stringent thymic central tolerance. Autoreactive B cell response against formiminotransferase-cyclodeaminase correlated with disease activity, possibly linking B-cell autoreactivity and AIH pathogenesis.ConclusionPeripheral tolerance and development of regulatory T cells after self-mimicking antigen exposure, and not sexual hormone nor central tolerance, are the main factors for susceptibility to AIH in females."xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.org/dc/terms/identifier | "doi:10.1002/hep.23536"xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/author | "Martin C."xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/author | "Lapierre P."xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/author | "Alvarez F."xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/author | "Beland K."xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/author | "Alvarez F. Jr."xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/date | "2010"xsd:gYear |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/name | "Hepatology"xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/pages | "1789-1798"xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/title | "Forkhead box p3+ regulatory T cell underlies male resistance to experimental type 2 autoimmune hepatitis."xsd:string |
| http://purl.uniprot.org/citations/20232291 | http://purl.uniprot.org/core/volume | "51"xsd:string |
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