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首页> 美国卫生研究院文献>Immunology >Presentation of the candidate rheumatoid arthritis autoantigen aggrecan by antigen-specific B cells induces enhanced CD4+ T helper type 1 subset differentiation
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Presentation of the candidate rheumatoid arthritis autoantigen aggrecan by antigen-specific B cells induces enhanced CD4+ T helper type 1 subset differentiation

机译：抗原特异性B细胞呈递候选类风湿性关节炎自身抗原聚集蛋白聚糖可诱导增强的CD4 + T辅助1型亚群分化

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Effective immune responses require antigen uptake by antigen-presenting cells (APC), followed by controlled endocytic proteolysis resulting in the generation of antigen-derived peptide fragments that associate with intracellular MHC class II molecules. The resultant peptide–MHC class II complexes then move to the APC surface where they activate CD4+ T cells. Dendritic cells (DC), macrophages and B cells act as efficient APC. In many settings, including the T helper type 1 (Th1) -dependent, proteoglycan-induced arthritis model of rheumatoid arthritis, accumulating evidence demonstrates that antigen presentation by B cells is required for optimal CD4+ T cell activation. The reasons behind this however, remain unclear. In this study we have compared the activation of CD4+ T cells specific for the proteoglycan aggrecan following antigen presentation by DC, macrophages and B cells. We show that aggrecan-specific B cells are equally efficient APC as DC and macrophages and use similar intracellular antigen-processing pathways. Importantly, we also show that antigen presentation by aggrecan-specific B cells to TCR transgenic CD4+ T cells results in enhanced CD4+ T cell interferon-γ production and Th1 effector sub-set differentiation compared with that seen with DC. We conclude that preferential CD4+ Th1 differentiation may define the requirement for B cell APC function in both proteoglycan-induced arthritis and rheumatoid arthritis.
机译：有效的免疫反应需要抗原呈递细胞（APC）吸收抗原，然后进行受控的胞吞蛋白水解作用，从而产生与细胞内MHC II类分子缔合的抗原衍生肽片段。然后，生成的II类MHC肽复合物移至APC表面，在其中激活CD4 + T细胞。树突状细胞（DC），巨噬细胞和B细胞可作为有效的APC。在许多情况下，包括类风湿性关节炎的T辅助型1（Th1）依赖性蛋白聚糖诱导的关节炎模型，越来越多的证据表明，最佳CD4 + T细胞活化需要B细胞呈递抗原。然而，其背后的原因尚不清楚。在这项研究中，我们比较了DC，巨噬细胞和B细胞在抗原呈递后对蛋白聚糖聚集蛋白聚糖具有特异性的CD4 + T细胞的活化。我们显示，聚集蛋白聚糖特异性B细胞与DC和巨噬细胞一样有效，并且使用类似的细胞内抗原加工途径。重要的是，我们还表明，聚集蛋白聚糖特异性B细胞向TCR转基因CD4 + T细胞呈递抗原会导致CD4 + T细胞干扰素-γ产生增强和Th1效应子集分化与DC相比。我们得出结论，CD4 + Th1的优先分化可能定义了蛋白聚糖诱发的关节炎和类风湿关节炎对B细胞APC功能的需求。

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