{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,20]],"date-time":"2026-10-20T21:37:10Z","timestamp":1792532230572,"version":"4.5.0"},"reference-count":29,"publisher":"National Academy of Sciences","issue":"51","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2013,12,17]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    In the human population different\n                    <jats:italic>HLA-C<\/jats:italic>\n                    allotypes are present that have different expression levels at the cell surface. Individuals with higher expressed\n                    <jats:italic>HLA-C<\/jats:italic>\n                    allotypes demonstrate better HIV control but increased risk of Crohn disease. A microRNA, miR-148a, regulates expression of some HLA-C allotypes. We report here that this microRNA also varies in expression level between people.\n                    <jats:italic>MIR148A<\/jats:italic>\n                    variation showed significant and opposing effects on HIV viral control vs. risk of Crohn disease, specifically in subjects with\n                    <jats:italic>HLA-C<\/jats:italic>\n                    alleles that are regulated by miR-148a. These results are independent of confounding effects by other\n                    <jats:italic>HLA<\/jats:italic>\n                    loci because only HLA-C is regulated by miR-148a. Our data represent an example of gene interactions that affect immune response and thereby the risk of human disease.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1312237110","type":"journal-article","created":{"date-parts":[[2013,11,18]],"date-time":"2013-11-18T23:49:39Z","timestamp":1384818579000},"page":"20705-20710","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":99,"title":["Genetic interplay between\n                    <i>HLA-C<\/i>\n                    and\n                    <i>MIR148A<\/i>\n                    in HIV control and Crohn disease"],"prefix":"10.1073","volume":"110","author":[{"given":"Smita","family":"Kulkarni","sequence":"first","affiliation":[{"name":"Cancer and Inflammation Program, Laboratory of Experimental Immunology and"},{"name":"Ragon Institute of Massachusetts General Hospital, Massachusetts Institute of Technology, and Harvard University, Cambridge, MA 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Switzerland;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George","family":"Nelson","sequence":"additional","affiliation":[{"name":"Basic Research Program, Center for Cancer Research Genetics Core, Science Applications International Corporation-Frederick, Inc., Frederick National Laboratory for Cancer Research, Frederick, MD 21702;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Haoyan","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University of California, San Francisco, CA 94115;"},{"name":"Department of Gastroenterology, Ren Ji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai Institute of Digestive Diseases, Shanghai 200001, China;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wilson","family":"Liao","sequence":"additional","affiliation":[{"name":"Department of Dermatology, University of California, San Francisco, CA 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