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Absolute reduction of peripheral regulatory T cell in patients with relapsing polychondritis


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

 

  1. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
  2. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
  3. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
  4. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
  5. Department of Rheumatology, the Second Hospital of Kunming Medical University, Kunming, Yunnan, China.
  6. Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
  7. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China.
  8. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, Shanxi, China. snwch@sina.com

CER13126
2021 Vol.39, N°3
PI 0487, PF 0493
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PMID: 32573423 [PubMed]

Received: 20/01/2020
Accepted : 05/05/2020
In Press: 23/06/2020
Published: 21/05/2021

Abstract

OBJECTIVES:
Although relapsing polychondritis (RP) is considered as an immune-mediated systemic disease, the levels of peripheral lymphocyte subpopulations are rarely studied in patients with RP. In this study, we focused on changes of peripheral CD4+T cell subsets in patients with RP.
METHODS:
Absolute numbers and percentages of CD4+T cell subsets including helper T(Th)1, Th2, Th17 cells and regulatory T (Treg) cells in peripheral blood (PB) from 19 RP patients, healthy controls and RA patients respectively were assessed by flow cytometry combined a microbead-based single-platform method. We compared the CD4+T cell levels in all RP patients and healthy controls. In addition, we analysed the difference of the absolute number and percentage of Treg cells between RP and RA patients.
RESULTS:
Compared with healthy controls, all RP patients had significantly both lower absolute number and proportion of Treg cells (absolute number, 45.10/μl vs. 22.48/μl, p<0.001; proportion, 5.19% vs. 3.78%, p<0.001) no matter whether they had received treatment or not. Similarly, the absolute number of Th2 cells in all RP patients was decreased (10.19/μl vs. 7.44/μl, p=0.030). However, there were no significant differences in percentages and absolute numbers of Th1 and Th17 cells between RP patients and healthy controls. The above results led to increased ratios of Th1/Treg (3.68 vs. 2.06, p=0.020), Th2/Treg (0.29 vs. 0.21, p=0.037) and Th17/Treg (0.25 vs. 0.14, p<0.001) in RP patients, and untreated RP patients were mainly characterised by the imbalance of Th17/Treg (0.25 vs. 0.14, p<0.01). There was no significant difference in Treg cells between RP and RA patients (p>0.05).
CONCLUSIONS:
Our data suggest that the reduction of Treg cells and its imbalance with Th cells play an important role in the pathogenesis of RP.

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