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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >Defective TLR9-driven STAT3 activation in B cells of patients with CVID
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Defective TLR9-driven STAT3 activation in B cells of patients with CVID

机译:CVID患者的B细胞中有缺陷TLR9驱动的STAT3活化

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摘要

B cell activation by Toll-like receptor 9 (TLR9) ligands is dependent on STAT3 and is important for optimal antibody responses to microbial antigens. B cells from patients with common variable immune deficiency (CVID) have impaired proliferation and differentiation in response to the TLR9 ligand CpG, despite normal levels of TLR9 expression. We demonstrate that CpG-driven STAT3 phosphorylation, but not activation of NFKB and p38, is selectively impaired in B cells from CVID patients. These results suggest that defective STAT3 activation contributes to the defective TLR9 and antibody response of B cells in CVID.
机译:通过Toll样受体9(TLR9)配体的B细胞活化取决于STAT3,对于对微生物抗原的最佳抗体反应是重要的。 尽管正常的TLR9表达水平,来自常见可变免疫缺陷患者(CVID)的患者来自常见的免疫缺乏症(CVID)的细胞患者响应于TLR9配体CPG而受损和分化。 我们证明CPG驱动的STAT3磷酸化,但未激活NFKB和P38,在来自CVID患者的B细胞中选择性地损害。 这些结果表明,缺陷的STAT3激活有助于CVID中B细胞的缺陷TLR9和抗体应答。

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