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Low-dose IL-2 effectively restored decreased regulatory T cells in patients with Behçet’s disease


1, 2, 3, 4, 5, 6

 

  1. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, China.
  2. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, China.
  3. Taiyuan University of Technology, Taiyuan, China.
  4. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, China.
  5. Department of Pathology, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA.
  6. Department of Rheumatology, the Second Hospital of Shanxi Medical University, Taiyuan, China. lxf_9859@sxmu.edu.cn

CER13221
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PMID: 32662405 [PubMed]

Received: 17/02/2020
Accepted : 05/06/2020
In Press: 10/07/2020

Abstract

OBJECTIVES:
Although Behçet’s disease (BD) is associated with immune mechanisms, the changes in circulating lymphocytes, especially regulatory T (Treg) cells remain unclear. Furthermore, low dose IL-2 has been reported to promote the expansion of Treg cells. This study aimed to investigate the significance of these subsets in the pathogenesis and the effect of low dose IL-2 on BD.
METHODS:
Lymphocyte subsets and cytokines from 177 BD patients and 160 healthy controls (HCs) were characterised. Then the efficacy and safety of low dose IL-2 for refractory BD patients were explored.
RESULTS:
There was a decrease in the absolute number of Treg cells and IL-10 in patients, while no difference in Th1, Th2, Th17 cells or their related cytokines. Accordingly, the ratio of Th17/Treg cells in patients was greatly higher than those of healthy controls. Furthermore, circulating Treg levels were negatively correlated with erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and Behçet’s disease current activity form (BDCAF), respectively. Lastly, after IL-2 treatment, all subsets were increased to some degree, while only Treg cells were amplified more dramatically, with a four-fold increase. Meanwhile, we found that the symptoms were mitigated without observed side effects.
CONCLUSIONS:
BD might be triggered by the defect of immunotolerance with decreased Treg. Moreover, low-dose IL-2 proposes a potential treatment by restoring Treg and promoting rapidly remission.

Rheumatology Article

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