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Autoimmune Valvular Carditis

  • AUTOIMMUNITY (TK TARRANT, SECTION EDITOR)
  • Published:
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Abstract

Autoimmune carditis is associated with many human rheumatic conditions, including rheumatic fever, systemic lupus erythematosus, and rheumatoid arthritis. The immune mechanisms that mediate the cardiovascular pathology connected to these diseases are poorly defined. Several animal models are used to recapitulate human pathophysiology in order to better characterize the immunopathogenic mechanisms driving autoimmune endocardial inflammation. These animal models point toward common mechanisms mediating autoimmune endocarditis; in particular, CD4+ T cells and pro-inflammatory macrophages play critical roles in directing the disease process. The goals of this review are to discuss the prevailing animal models of autoimmune endocarditis and their underlying immunologic mechanisms and to provide insight regarding potential therapeutic targets in humans.

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Acknowledgments

Research in Dr. Binstadt’s laboratory was funded by the National Institutes of Health (NIH), National Heart, Lung, and Blood Institute R01 HL121093; National Institute of Arthritis and Musculoskeletal and Skin Diseases R03 AR057101; an Innovative Research Grant from the Rheumatology Research Foundation; and by the University of Minnesota Department of Pediatrics. Ms. Breed is a student in the University of Minnesota Medical Scientist Training Program supported by NIH T32 GM008244.

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Conflict of Interest

Ms. Breed and Dr. Binstadt report grants from the NIH, the National Heart, Lung and Blood Institute, the National Institute of Arthritis and Musculoskeletal and Skin Diseases, and the Rheumatology Research Foundation.

Human and Animal Rights and Informed Consent

This article does not contain any studies with human or animal subjects performed by the authors.

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Correspondence to Bryce A. Binstadt.

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This article is part of the Topical Collection on Autoimmunity

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Breed, E.R., Binstadt, B.A. Autoimmune Valvular Carditis. Curr Allergy Asthma Rep 15, 491 (2015). https://doi.org/10.1007/s11882-014-0491-z

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