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Nat Immunol.:TBK1通过NF-κB 通路调节IgA数量

来源:中国科学报 2012-10-26 00:02

近期《自然—免疫学》上的一项研究为我们揭示了小鼠身体是如何限制IgA抗体在血液循环中的数量,从而降低肾脏患病风险的。这或许有助于为那些受到IgA调控下的自体免疫折磨的患者开发新的干预疗法。

Shao-Cong Sun等人对产生抗体的细胞——B免疫细胞进行了研究。B细胞的活跃能够增加抗体产量并引发免疫球蛋白类别转换过程,从而决定抗体的最终类型。研究人员发现一种名为TBK1的调节分子能够阻止向IgA的转变。一旦小鼠的B细胞缺乏TBK1表达,其体内血清会产生更大量的IgA,包括可针对自身组织的抗体。随着自体免疫IgA复合物在肾脏中的积累,小鼠会产生肾功能障碍以及与IgA有关的人类患病症状。(生物谷Bioon.com)

The kinase TBK1 controls IgA class switching by negatively regulating noncanonical NF-κB signaling

Jin J, Xiao Y, Chang JH, Yu J, Hu H, Starr R, Brittain GC, Chang M, Cheng X, Sun SC.

Immunoglobulin class switching is crucial for the generation of antibody diversity in humoral immunity and, when deregulated, also has severe pathological consequences. How the magnitude of immunoglobulin isotype switching is controlled is still poorly understood. Here we identify the kinase TBK1 as a pivotal negative regulator of class switching to the immunoglobulin A (IgA) isotype. B cell-specific ablation of TBK1 in mice resulted in uncontrolled production of IgA and the development of nephropathy-like disease signs. TBK1 negatively regulated IgA class switching by attenuating noncanonical signaling via the transcription factor NF-κB, an action that involved TBK1-mediated phosphorylation and subsequent degradation of the NF-κB-inducing kinase NIK. Our findings establish TBK1 as a pivotal negative regulator of the noncanonical NF-κB pathway and identify a unique mechanism that controls IgA production

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