{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T02:45:38Z","timestamp":1787021138253,"version":"build-2736575974"},"reference-count":99,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2017,12,29]],"date-time":"2017-12-29T00:00:00Z","timestamp":1514505600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2018,2,27]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Because of their vital function, the wall structures of medium and large arteries are immunoprivileged and protected from inflammatory attack. That vascular immunoprivilege is broken in atherosclerosis and in vasculitis, when wall-invading T cells and macrophages (M\u03d5) promote tissue injury and maladaptive repair. Historically, tissue-residing T cells were studied for their antigen specificity, but recent progress has refocused attention to antigen-nonspecific regulation, which determines tissue access, persistence, and functional differentiation of T cells. The coinhibitory receptor PD-1, expressed on T cells, delivers negative signals when engaged by its ligand PD-L1, expressed on dendritic cells, M\u03d5, and endothelial cells to attenuate T cell activation, effector functions, and survival. Through mitigating signals, the PD-1 immune checkpoint maintains tissue tolerance. In line with this concept, dendritic cells and M\u03d5s from patients with the vasculitic syndrome giant cell arteritis (GCA) are PD-L1lo; including vessel-wall\u2013embedded DCs that guard the vascular immunoprivilege. GCA infiltrates in the arterial walls are filled with PD-1+ T cells that secrete IFN-\u03b3, IL-17, and IL-21; drive inflammation-associated angiogenesis; and facilitate intimal hyperplasia. Conversely, chronic tissue inflammation in the atherosclerotic plaque is associated with an overreactive PD-1 checkpoint. Plaque-residing M\u03d5s are PD-L1hi, a defect induced by their addiction to glucose and glycolytic breakdown. PD-L1hi M\u03d5s render patients with coronary artery disease immunocompromised and suppress antiviral immunity, including protective anti\u2013varicella zoster virus T cells. Thus, immunoinhibitory signals affect several domains of vascular inflammation; failing PD-L1 in vasculitis enables unopposed immunostimulation and opens the flood gates for polyfunctional inflammatory T cells, and excess PD-L1 in the atherosclerotic plaque disables tissue-protective T cell immunity.<\/jats:p>","DOI":"10.1189\/jlb.3ma0717-283","type":"journal-article","created":{"date-parts":[[2017,8,28]],"date-time":"2017-08-28T20:25:26Z","timestamp":1503951926000},"page":"565-575","source":"Crossref","is-referenced-by-count":76,"title":["The immunoinhibitory PD-1\/PD-L1 pathway in inflammatory blood vessel disease"],"prefix":"10.1093","volume":"103","author":[{"given":"Cornelia M","family":"Weyand","sequence":"first","affiliation":[{"name":"Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine , Stanford, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gerald J","family":"Berry","sequence":"additional","affiliation":[{"name":"Department of Pathology, Stanford University School of Medicine , Stanford, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00f6rg J","family":"Goronzy","sequence":"additional","affiliation":[{"name":"Division of Immunology and Rheumatology, Department of Medicine, Stanford University School of Medicine , Stanford, California, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2017,12,29]]},"reference":[{"key":"2023013012241148200_jlb10060-bib-0001","doi-asserted-by":"crossref","first-page":"3847","DOI":"10.1007\/s00018-013-1289-1","article-title":"Inflammation and immune system interactions in atherosclerosis","volume":"70","author":"Legein","year":"2013","journal-title":"Cell. 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