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Updated: Jul 18, 2026

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis
06:35

An Immunohistopathologic Study to Profile the Folate Receptor Beta Macrophage and Vascular Immune Microenvironment in Giant Cell Arteritis

Published on: February 8, 2019

Giant cell and Takayasu arteritis

Yoshinori Seko1

  • 1Department of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo, Japan. sekoyosh-tky@umin.ac.jp

Current Opinion in Rheumatology
|December 5, 2006
PubMed

Insights

Recent advances in large vessel vasculitis research highlight new imaging techniques for monitoring disease activity and potential genetic links to giant cell arteritis (GCA) and Takayasu arteritis (TA). Antitumor necrosis factor-alpha therapies show promise for refractory cases.

Area of Science:

  • Rheumatology
  • Immunology
  • Radiology

Background:

  • Giant cell arteritis (GCA) and Takayasu arteritis (TA) are large vessel vasculitides with unknown causes.
  • Both conditions share similar clinical manifestations, necessitating a review of recent findings.

Purpose of the Study:

  • To review recent clinical and pathophysiological advances in GCA and TA.
  • To focus on research published within the past year.

Main Methods:

  • Review of recent scientific literature on GCA and TA.
  • Analysis of imaging techniques, including delayed gadolinium-enhanced MRI.
  • Examination of genetic association studies and therapeutic advancements.

Main Results:

  • Delayed gadolinium-enhanced MRI shows potential for monitoring aortic wall inflammation in TA and small vessel inflammation in GCA.
  • Antitumor necrosis factor-alpha monoclonal antibody therapy demonstrates efficacy in patients resistant to standard treatments.
  • Gene polymorphisms in inducible nitric oxide synthase and I-kappaB-like protein are associated with susceptibility to GCA and TA, respectively.

Conclusions:

  • Advanced imaging techniques offer improved evaluation of vascular lesion activity and treatment guidance for GCA and TA.
  • Further elucidation of pathophysiological mechanisms may lead to novel targeted therapies, such as anti-TNF-alpha agents.
Abstract

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