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Circulating TFH cells is correlated with disease activity in anti-MDA5 antibody positive idiopathic inflammatory myopathies


1, 2, 3, 4, 5, 6, 7, 8

 

  1. Department of Rheumatology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
  2. Department of Rheumatology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
  3. Department of Rheumatology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
  4. Department of Rheumatology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
  5. Department of Rheumatology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
  6. Department of Rheumatology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
  7. Department of Rheumatology, and Institute of Precision Medicine,The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China.
  8. Department of Rheumatology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, China. zsuyns@163.com

CER13288
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PMID: 32896262 [PubMed]

Received: 06/03/2020
Accepted : 01/07/2020
In Press: 03/09/2020

Abstract

OBJECTIVES:
Idiopathic inflammatory myopathies (IIM) are a group of disorders characterised by the production of autoantibodies and inflammatory infiltrates in the skeletal muscles. Follicular T helper (TFH) cells are known to be crucial for B cell differentiation and autoantibody production in autoimmune diseases. The aim of this study was to investigate the involvement of TFH cells in IIM.
METHODS:
Circulating TFH cells in 44 IIM patients or 11 age- and gender-matched healthy controls (HCs) were measured by flow cytometry. ICOS, PD-1, active caspase-1 and Ki-67 expression in TFH cells was examined. The correlations between the frequency of TFH cells and clinical disease activities were also analysed.
RESULTS:
The frequency of TFH cells was 16.6% in IIM patients with anti-melanoma differentiation-associated gene (MDA5) antibody compared to 10.6% and 12.9% in anti-MDA5 negative patients or HCs, respectively (both p<0.05). The frequency of TFH cells was positively correlated with clinical disease activities: patient/parent’s assessment VAS (r=0.51, p<0.05), physician’s assessment VAS (r=0.59, p<0.05) and MYOACT scores (total systems: r=0.62, p<0.05; extramuscular system: r=0.56, p<0.05; pulmonary system, r=0.55, p<0.05). The percentage of PD-1highICOShigh TFH cells was 3.68% in anti-MDA5 positive patients compared to 2.70% and 1.96% in anti-MDA5 negative patients or HCs, respectively (both p<0.05). The percentage of Ki-67 positive TFH cells was 3.50% in anti-MDA5 positive patients compared to 2.36% and 1.76% in anti-MDA5 negative patients or HCs, respectively (p<0.05). Interestingly, active caspase-1 was significantly increased in TFH cells in anti-MDA5 positive patients compared to the patients without anti-MDA5 or HCs (3.30% vs. 1.67% and 3.30% vs. 1.02%, both p<0.001).
CONCLUSIONS:
These data suggest a role for TFH cells in the pathogenesis of anti-MDA5 positive IIM and TFH cells might serve as a disease biomarker for this subset of patients.

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