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

LJ Chi, HB Wang, WZ Wang - Journal of the Peripheral …, 2008 - Wiley Online Library
LJ Chi, HB Wang, WZ Wang
Journal of the Peripheral Nervous System, 2008Wiley Online Library
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 …
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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