NDLI: Immunoinhibitory checkpoint deficiency in medium and large vessel vasculitis

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Immunoinhibitory checkpoint deficiency in medium and large vessel vasculitis

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Immunoinhibitory checkpoint deficiency in medium and large vessel vasculitis

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Watanabe, Ryu Goronzy, Jörg J. Zhang, Hui Weyand, Cornelia M. Vaglio, Augusto Warrington, Kenneth J. Liao, Yaping Joyce Berry, Gerald J.
Description	Author Affiliation: Zhang H ( Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA 94305.); Watanabe R ( Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA 94305.); Berry GJ ( Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305.); Vaglio A ( Division of Nephrology, University Hospital of Parma, 43100 Parma, Italy.); Liao YJ ( Department of Ophthalmology, Stanford Byers Eye Institute, Stanford University School of Medicine, Stanford, CA 94305.); Warrington KJ ( Division of Rheumatology, Mayo Clinic College of Medicine, Rochester, MN 55905.); Goronzy JJ ( Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA 94305.); Weyand CM ( Department of Medicine, Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, CA 94305);
Abstract	Giant cell arteritis (GCA) causes autoimmune inflammation of the aorta and its large branches, resulting in aortic arch syndrome, blindness, and stroke. $CD4^{+}$ T cells and macrophages form organized granulomatous lesions in the walls of affected arteries, destroy the tunica media, and induce ischemic organ damage through rapid intimal hyperplasia and luminal occlusion. Pathogenic mechanisms remain insufficiently understood; specifically, it is unknown whether the unopposed activation of the immune system is because of deficiency of immunoinhibitory checkpoints. Transcriptome analysis of GCA-affected temporal arteries revealed low expression of the coinhibitory ligand programmed death ligand-1 (PD-L1) concurrent with enrichment of the programmed death-1 (PD-1) receptor. Tissue-residing and ex vivo-generated dendritic cells (DC) from GCA patients were $PD-L1^{lo},$ whereas the majority of vasculitic T cells expressed PD-1, suggesting inefficiency of the immunoprotective PD-1/PD-L1 immune checkpoint. DC–PD-L1 expression correlated inversely with clinical disease activity. In human artery-SCID chimeras, PD-1 blockade exacerbated vascular inflammation, enriched for $PD-1^{+}$ effector T cells, and amplified tissue production of multiple T-cell effector cytokines, including IFN-γ, IL-17, and IL-21. Arteries infiltrated by $PD-1^{+}$ effector T cells developed microvascular neoangiogenesis as well as hyperplasia of the intimal layer, implicating T cells in the maladaptive behavior of vessel wall endogenous cells. Thus, in GCA, a breakdown of the tissue-protective PD1/PD-L1 checkpoint unleashes vasculitic immunity and regulates the pathogenic remodeling of the inflamed arterial wall.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	6
Volume Number	114
Language	English
Publisher	National Academy of Sciences
Publisher Date	2017-01-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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