IL-35 Is Involved in the Pathogenesis of Guillain-Barré Syndrome Through Its Influence on the Function of CD4+ T Cells.

Capa:IL-35 Is Involved in the Pathogenesis of Guillain-Barré Syndrome Through Its Influence on the Function of CD4+ T Cells.

Autor(es): Liu Hao; Zhang Wei; Tian Fa-Fa; Kun Na; Zhou Wen-Bin; Xiao Bo; Li Jing


Resumo: CD4+ T cells and many cytokines play critical roles in the pathogenesis of Guillain-Barré Syndrome (GBS), an immune-mediated inflammatory disease. However, the role of IL-35, a novel member of the IL-12 cytokine family, in this kind of disease has not yet been elucidated. In this study, we investigated the functional changes of CD4+ T cells from GBS patients with IL-35 treatment in vitro. This study involved 21 GBS patients and an equal number of healthy controls (HCs). The results indicated that the average concentration of IL-35 in the plasma of GBS patients was lower than that of healthy controls (HCs). Increased levels of STAT1, STAT3 and STAT4 proteins and T-bet, ROR ?t, IFN-? and IL-17A mRNA were observed in CD4+ T cells from GBS patients. In contrast, the levels of STAT5 and STAT6 proteins and GATA3, Foxp3, IL-4 and TGF-?1 mRNAs were decreased in GBS patients in comparison with those of HCs. In addition, treatment of CD4+ T cells from GBS patients with IL-35 upregulated IL-35, STAT5 and STAT6 protein and T-bet, GATA3, Foxp3, IFN-?, IL-4, IL-17A and TGF-?1 mRNA while inhibited levels of STAT3 and STAT4 protein and ROR?t and IL-17A mRNA. These results indicate that IL-35 might play a potential role in GBS pathogenesis. Further studies are required in order to evaluate its role in GBS.


Palavras-Chave: CD4+ T cells, Guillain-Barré Syndrome, IL-35, STAT, transcription factors


Imprenta: Immunological Investigations, v. 44, n. 6, p. 566-77, 2015


Identificador do objeto digital: 10.3109/08820139.2015.1043671


Descritores: Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Cytokines


Data de publicação: 2015