Impairment of circulating CD4+CD25+ regulatory T cells in patients with chronic inflammatory demyelinating polyradiculoneuropathy

Authors

  • Li-Jun Chi,

    1. Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin
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  • Hua-Bing Wang,

    1. Department of Neurology, Peking Union Medical College Hospital, Peking, China
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  • Wei-Zhi Wang

    Corresponding author
    1. Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin
      Wei-Zhi Wang, MD, Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China. Tel: +86 13895783757; Fax: +86-451-86605656; E-mail: clj.3757@yahoo.com.cn
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Wei-Zhi Wang, MD, Department of Neurology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150086, China. Tel: +86 13895783757; Fax: +86-451-86605656; E-mail: clj.3757@yahoo.com.cn

Abstract

Abstract  Chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) is an immune-mediated peripheral nervous system disease. CD4+CD25+ T regulatory cells (Tregs) have been unequivocally shown to be critical in maintaining immune tolerance and preventing auto-immune diseases by suppressing self-reactive T cells. Thus, we hypothesized that the numbers and/or the function of Tregs would be deranged during the progressive or relapse phases of CIDP. The number of Tregs was determined by flow cytometry according to their characteristic CD4+CD25high membrane phenotype. Functional characterization of Tregs was analyzed by suppression of proliferation and secretion of cytokines by co-cultured effector CD4+CD25 T cells. FOXP3 message expression level was assessed by quantitative real-time polymerase chain reaction. The results showed significant reduction in both the number and the suppressive function of Tregs in the patients with CIDP compared with healthy controls. Also, Tregs isolated from CIDP patients expressed lower levels of FoxP3 mRNA. During the progressive or the relapsing phases of CIDP, the number of Tregs was reduced, and the suppressive function of them decreased. These findings may be helpful to our understanding of the possible role of Tregs in the pathogenesis of CIDP.

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