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Pathogenesis of Giant Cell Arteritis and Takayasu Arteritis—Similarities and Differences

  • Recent Advances in Large Vessel Vasculitis (C Dejaco and C Duftner, Section Editors)
  • Published:
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Abstract

Purpose of Review

Giant cell arteritis (GCA) and Takayasu arteritis (TAK) are auto-inflammatory and autoimmune diseases with a highly selective tissue tropism for medium and large arteries. In both diseases, CD4+ T cells and macrophages form granulomatous lesions within the arterial wall, a tissue site normally protected by immune privilege. Vascular lesions can be accompanied by an extravascular component, typically an intense hepatic acute phase response that produces well-known laboratory abnormalities, e.g., elevated ESR and CRP. It is unclear whether GCA and TAK lie on a spectrum of disease or whether they represent fundamentally different disease processes.

Recent Findings

GCA and TAK share many clinical features, but there are substantial differences in genetics, epidemiology, disease mechanisms, response to treatment, and treatment complications that give rise to different disease trajectories. A significant difference lies in the composition of the wall-infiltrating immune cell compartment, which in TAK includes a significant population of CD8+ T cells as well as natural killer cells, specifying disparate disease effector pathways mediating tissue damage and vessel wall remodeling.

Summary

Despite the similarities in tissue tropism and histomorphology, GCA and TAK are two distinct vasculitides that rely on separate disease mechanisms and require disease-specific approaches in diagnosis and management.

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Funding

This work was supported by the National Institutes of Health (R01 AR042547, R01 HL117913, R01 AI108906, R01 HL142068, and P01 HL129941 to CMW and R01 AI108891, R01 AG045779, U19 AI057266, R01 AI129191, and I01 BX001669 to JJG) and with resources and the use of facilities at the Palo Alto Veterans Administration Healthcare System.

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  1. Ryu Watanabe

    Present address: Department of Advanced Medicine for Rheumatic Diseases, Kyoto University Graduate School of Medicine, Kyoto, Japan

Authors and Affiliations

  1. Department of Medicine, Stanford University School of Medicine, CCSR Building Room 2225, 269 Campus Drive West, Stanford, CA, 94305-5166, USA

    Ryu Watanabe, David H. Liang, Jörg J. Goronzy & Cornelia M. Weyand

  2. Department of Pathology, Stanford University School of Medicine, Stanford, CA, 94305, USA

    Gerald J. Berry

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Watanabe, R., Berry, G.J., Liang, D.H. et al. Pathogenesis of Giant Cell Arteritis and Takayasu Arteritis—Similarities and Differences. Curr Rheumatol Rep 22, 68 (2020). https://doi.org/10.1007/s11926-020-00948-x

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