{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,30]],"date-time":"2026-09-30T03:49:19Z","timestamp":1790740159803,"version":"4.1.0"},"reference-count":44,"publisher":"Oxford University Press (OUP)","issue":"2","license":[{"start":{"date-parts":[[2011,7,1]],"date-time":"2011-07-01T00:00:00Z","timestamp":1309478400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2011,7,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>Chronic allograft vasculopathy (CAV) contributes to heart transplant failure, yet its pathogenesis is incompletely understood. Although cellular and humoral alloimmunity are accepted pathogenic mediators, animal models suggest that T cells and Abs reactive to graft-expressed autoantigens, including cardiac myosin (CM), could participate. To test the relationship between CAV and anti-CM autoimmunity in humans, we performed a cross-sectional study of 72 heart transplant recipients: 40 with CAV and 32 without. Sera from 65% of patients with CAV contained anti-CM Abs, whereas &amp;lt;10% contained Abs to other autoantigens (p &amp;lt; 0.05), and only 18% contained anti-HLA Abs (p &amp;lt; 0.05 versus anti-CM). In contrast, 13% of sera from patients without CAV contained anti-CM Abs (p &amp;lt; 0.05; odds ratio [OR], associating CAV with anti-CM Ab = 13, 95% confidence interval [CI] 3.79\u201344.6). Multivariable analysis confirmed the association to be independent of time posttransplant and the presence of anti-HLA Abs (OR = 28, 95% CI 5.77\u2013133.56). PBMCs from patients with CAV responded more frequently to, and to a broader array of, CM-derived peptides than those without CAV (p = 0.01). Detection of either CM\u2013peptide-reactive T cells or anti-CM Abs was highly and independently indicative of CAV (OR = 45, 95% CI 4.04\u2013500.69). Our data suggest detection of anti-CM immunity could be used as a biomarker for outcome in heart transplantation recipients and support the need for further studies to assess whether anti-CM immunity is a pathogenic mediator of CAV.<\/jats:p>","DOI":"10.4049\/jimmunol.1004195","type":"journal-article","created":{"date-parts":[[2011,6,16]],"date-time":"2011-06-16T13:45:17Z","timestamp":1308231917000},"page":"1023-1030","source":"Crossref","is-referenced-by-count":61,"title":["Anticardiac Myosin Immunity and Chronic Allograft Vasculopathy in Heart Transplant Recipients"],"prefix":"10.1093","volume":"187","author":[{"given":"Safa","family":"Kalache","sequence":"first","affiliation":[{"name":"Department of Medicine, Mount Sinai School of Medicine , New York, NY 10029"},{"name":"Division of Nephrology, Mount Sinai School of Medicine , New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rajani","family":"Dinavahi","sequence":"additional","affiliation":[{"name":"Department of Medicine, Mount Sinai School of Medicine , New York, NY 10029"},{"name":"Division of Nephrology, Mount Sinai School of Medicine , New York, NY 10029"},{"name":"Recanati\/Miller Transplant Institute, Mount Sinai School of Medicine , New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sean","family":"Pinney","sequence":"additional","affiliation":[{"name":"Department of Medicine, Mount Sinai School of Medicine , New York, NY 10029"},{"name":"Recanati\/Miller Transplant Institute, Mount Sinai School of Medicine , New York, NY 10029"},{"name":"Division of Cardiology, Mount Sinai School of Medicine , New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anita","family":"Mehrotra","sequence":"additional","affiliation":[{"name":"Department of Medicine, Mount Sinai School of Medicine , New York, NY 10029"},{"name":"Division of Nephrology, Mount Sinai School of Medicine , New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Madeleine W","family":"Cunningham","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Oklahoma , Oklahoma City, OK 73126"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter S","family":"Heeger","sequence":"additional","affiliation":[{"name":"Department of Medicine, Mount Sinai School of Medicine , New York, NY 10029"},{"name":"Division of Nephrology, Mount Sinai School of Medicine , New York, NY 10029"},{"name":"Recanati\/Miller Transplant Institute, Mount Sinai School of Medicine , New York, NY 10029"},{"name":"Immunology Institute, Mount Sinai School of Medicine , New York, NY 10029"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2011,7,15]]},"reference":[{"key":"2025032410230350800_r1","doi-asserted-by":"crossref","first-page":"e116","DOI":"10.2741\/johnston","article-title":"Overcoming cardiac allograft vasculopathy (CAV) by inducing tolerance","volume":"7","author":"Johnston","year":"2002","journal-title":"Front. 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