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

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

Research output: Contribution to journalReview articlepeer-review

6 Scopus citations


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.

Original languageEnglish (US)
Article number68
JournalCurrent rheumatology reports
Issue number10
StatePublished - Oct 1 2020


  • Giant cell arteritis
  • Intimal hyperplasia
  • Macrophages
  • Neoangiogenesis
  • T cells
  • T regulatory cells
  • Takayasu arteritis
  • Vascular remodeling

ASJC Scopus subject areas

  • Rheumatology


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