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Large-vessel vasculitis

 

Contribution of Th2-like Treg cells to the pathogenesis of Takayasu’s arteritis


1, 2, 3, 4, 5, 6

 

  1. Department of Rheumatology, Capital Medical University Affiliated Anzhen Hospital, Beijing, China.
  2. Department of Rheumatology, Capital Medical University Affiliated Anzhen Hospital, Beijing, and Beijing Institute of Heart, Lung and Vessel Disease, China.
  3. Department of Rheumatology, Capital Medical University Affiliated Anzhen Hospital, Beijing, and Beijing Institute of Heart, Lung and Vessel Disease, China.
  4. Department of Rheumatology, Capital Medical University Affiliated Anzhen Hospital, Beijing, China.
  5. Department of Rheumatology, Capital Medical University Affiliated Anzhen Hospital, Beijing, and Beijing Institute of Heart, Lung and Vessel Disease, China.
  6. Department of Rheumatology, Capital Medical University Affiliated Anzhen Hospital, Beijing, China. lilypansxmu@sina.com

CER12482
2020 Vol.38, N°2 ,Suppl.124
PI 0048, PF 0054
Large-vessel vasculitis

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PMID: 31969221 [PubMed]

Received: 06/06/2019
Accepted : 02/09/2019
In Press: 14/01/2020
Published: 21/05/2020

Abstract

OBJECTIVES:
Takayasu’s arteritis (TAK) involves inflammatory vasculitis of large vessels and mainly affects the aorta and its major branches. Abnormal immunity may play a vital role in TAK pathogenesis. Regulatory T cells (Treg cells) are important for peripheral tolerance, but under certain conditions Treg cells can differentiate into Th-like cells that have lost immune suppressive function and promote the development of autoimmune diseases. The role of Th-like Treg cells in TAK is unclear and this study aims to investigate the function of Th-like Treg cell subsets and associated cytokines in TAK.
METHODS:
A total of 51 patients with TAK and 32 healthy controls were enrolled. The percentage of Th1, Th2, Th17, Tregs and Th-like Treg cells in blood samples was analyzed by flow cytometry. Serum cytokine levels were detected using a cytometric bead array for cytokines.
RESULTS:
TAK patients had decreased numbers of Th2-like Treg cells in the peripheral blood (p=0.002) relative to healthy controls. The percentage of Treg cells in samples from TAK patients also decreased (p=0.002), but the Th2 cell percentage (p=0.04) increased compared to healthy controls. TAK patients had higher serum levels of IL-4 (p<0.001) and IL-13 (p<0.001) than healthy controls, and levels of both cytokines correlated to IL-6 levels.
CONCLUSIONS:
We studied changes in T helper-like Treg cell subsets in TAK for the first time and discovered that the number of Th2-like Treg cells in peripheral blood decreased. Results of this study suggested that Th2-like Treg cells could contribute to TAK pathogenesis.

Rheumatology Article