小柯机器人

澳大利亚国立大学Carola G. Vinuesa研究小组发现，卵泡调节性T细胞产生神经突蛋白来调节B细胞。2021年3月11日，国际知名学术期刊《细胞》在线发表了这一成果。

研究人员发现，表达BCL6的Treg，称为卵泡调节性T（Tfr）细胞，可产生靶向B细胞的丰富神经氨酸蛋白。缺乏Tfr细胞的小鼠或在表达Foxp3的细胞中缺乏神经突蛋白的小鼠在生发中心（GC）中积累了早期浆细胞，并形成了针对组蛋白和组织特异性自身抗原的自身抗体。免疫后，这些小鼠还产生增加的血浆IgE和IgG1。

研究人员发现，神经突蛋白被B细胞吸收，引起许多蛋白质的磷酸化，并抑制IgE类型转换。神经突蛋白减少了小鼠和人类GC B细胞向浆细胞的分化，BLIMP-1的下调和BCL6的上调。向Tfr缺陷型小鼠注射神经突蛋白可防止早期血浆细胞在GC中积聚。Tfr细胞产生的神经突蛋白是抑制B细胞驱动自身免疫和IgE介导过敏的主要机制。 

据了解，调节性T细胞可防止自身抗体和过量IgE的出现，但确切的机制尚不清楚。

附：英文原文

Title: Follicular regulatory T cells produce neuritin to regulate B cells

Author: Paula Gonzalez-Figueroa, Jonathan A. Roco, Ilenia Papa, Lorena Núez Villacís, Maurice Stanley, Michelle A. Linterman, Alexander Dent, Pablo F. Canete, Carola G. Vinuesa

Issue&Volume: 2021-03-11

Abstract: Regulatory T cells prevent the emergence of autoantibodies and excessive IgE, butthe precise mechanisms are unclear. Here, we show that BCL6-expressing Tregs, knownas follicular regulatory T (Tfr) cells, produce abundant neuritin protein that targetsB cells. Mice lacking Tfr cells or neuritin in Foxp3-expressing cells accumulatedearly plasma cells in germinal centers (GCs) and developed autoantibodies againsthistones and tissue-specific self-antigens. Upon immunization, these mice also producedincreased plasma IgE and IgG1. We show that neuritin is taken up by B cells, causesphosphorylation of numerous proteins, and dampens IgE class switching. Neuritin reduceddifferentiation of mouse and human GC B cells into plasma cells, downregulated BLIMP-1,and upregulated BCL6. Administration of neuritin to Tfr-deficient mice prevented theaccumulation of early plasma cells in GCs. Production of neuritin by Tfr cells emergesas a central mechanism to suppress B cell-driven autoimmunity and IgE-mediated allergies.

DOI: 10.1016/j.cell.2021.02.027

Source: https://www.cell.com/cell/fulltext/S0092-8674(21)00177-X