调节性B细胞
CD38
CD19
免疫学
B细胞
白细胞介素10
乙型肝炎病毒
乙型肝炎
T细胞
CD24型
生物
医学
细胞
细胞因子
免疫系统
抗体
病毒
细胞生物学
干细胞
遗传学
CD44细胞
川地34
作者
YaYun Liu,Ying Luo,Tong Zhu,Meng Jiang,Zhao Feng Tian,Gusheng Tang,Xuesong Liang
标识
DOI:10.3389/fimmu.2021.653198
摘要
Interleukin (IL)-35-secreting B (IL-35+B) cells are critical regulators in autoimmune and infectious diseases and exert suppressive functions in parallel with IL-10-producing B (B10) cells. However, the role of IL-35+B cells in persistent hepatitis B virus (HBV) infection remains unclear. To elucidate the role of IL-35+B cells in the progress of chronic HBV infection, we determined the frequency of IL-35+B cells and their relationship with the classical human regulatory B cell (Breg) subsets, namely, CD19+CD24 hi CD38 hi and CD19+CD24 hi CD27+. Then, the regulatory effect and mechanism of Bregs on effector T cells were investigated in vitro . Here, we found that compared with healthy controls, the frequency of IL-35+B cells was increased in patients with chronic HBV infection and was enriched in human classical Breg subset CD19+CD24 hi CD38 hi B cells. Moderate correlation was observed between the frequency of IL-35+B cells and alanine aminotransferase levels (Spearman r = 0.401), but only mild correlation was noted between the frequency of IL-35+B cells and HBV DNA level (Spearman r = 0.314). The frequency of IL-35+B cells was negatively correlated with interferon-γ (IFN-γ)-producing CD4+ and CD8+ cells but positively correlated with IL-4-producing T cells. Bregs dysregulated T cell function through an IL-35-dependent mechanism and depended on cell-to-cell contact. In conclusion, IL-35+ B cell was enriched in CD19+CD24hiCD38hi B cell subset during persistent HBV infection and Breg cells exerted dysregulation in T cell function through IL-35 dependent mechanism and depend on cell-to-cell contact. Clinical Trial Registration www.ClinicalTrials.gov , identifier NCT03734783.
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