Marginal zone (MZ) B cells are innate‐like B cells that produce polyreactive antibodies with an affinity for microbial molecular patterns and carbohydrate ligands. MZ B cells have been shown to be important in mediating immunity to various bacteria including Streptococcus pneumoniae and are also implicated in inflammatory syndromes including lupus erythematosus. The intestinal microbiota is responsible for producing short‐chain fatty acids, which can regulate immune cell function by several mechanisms including ligation of the G‐protein‐coupled receptor (GPR)43. Herein, we show that MZ B cells express Gpr43 messenger RNA and that the absence of this receptor impacts on MZ B‐cell surface marker expression and antibody production. In T‐cell‐independent responses to the hapten 4‐hydroxy‐3‐nitrophenylacetic acid (NP), mice deficient in GPR43 displayed higher serum titers of NP‐specific antibodies. Moreover, in response to a pneumococcal polysaccharide vaccine, GPR43‐deficient mice developed robust serum antibody responses and had markedly increased numbers of splenic antibody‐secreting cells, compared with control mice. Finally, serum immunoglobulin M autoantibodies to double‐stranded DNA and phosphatidylcholine were increased in resting 10–15‐week‐old mice lacking GPR43. Taken together, mice lacking GPR43 have heightened antibody responses to T‐cell‐independent antigens, which may be a result of impaired regulation of MZ B cells.

中文翻译：

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GPR43 调节边缘区 B 细胞对外来和内源性抗原的反应

边缘区 (MZ) B 细胞是先天性 B 细胞，可产生对微生物分子模式和碳水化合物配体具有亲和力的多反应性抗体。MZ B 细胞已被证明在介导对包括肺炎链球菌在内的各种细菌的免疫方面很重要，并且还与包括红斑狼疮在内的炎症综合征有关。肠道微生物群负责产生短链脂肪酸，短链脂肪酸可以通过多种机制调节免疫细胞功能，包括 G 蛋白偶联受体 (GPR) 43 的连接。在此，我们显示 MZ B 细胞表达Gpr43信使 RNA，并且该受体的缺失会影响 MZ B 细胞表面标志物的表达和抗体的产生。在对半抗原 4-羟基-3-硝基苯乙酸 (NP) 的 T 细胞非依赖性反应中，缺乏 GPR43 的小鼠表现出更高的 NP 特异性抗体血清滴度。此外，针对肺炎球菌多糖疫苗，与对照小鼠相比，GPR43 缺陷小鼠产生了强烈的血清抗体反应，并且脾抗体分泌细胞的数量显着增加。最后，在缺乏 GPR43 的静息 10-15 周龄小鼠中，针对双链 DNA 和磷脂酰胆碱的血清免疫球蛋白 M 自身抗体增加。总之，缺乏 GPR43 的小鼠对 T 细胞非依赖性抗原的抗体反应增强，这可能是 MZ B 细胞调节受损的结果。