Diet‐induced obesity is associated with impaired B‐cell‐driven humoral immunity, which coincides with chronic inflammation and has consequences for responses to infections and vaccinations. Key nutritional, cellular, and molecular mechanisms by which obesity may impair aspects of humoral immunity such as B cell development, class switch recombination, and formation of long‐lived antibody secreting cells are reviewed. A key theme to emerge is the central role of white adipose tissue on the formation and function of pro‐inflammatory B cell subsets that exacerbate insulin resistance. The underlying role of select hormones such as leptin is highlighted, which may be driving the formation of pro‐inflammatory B cells in the absence of antigen stimulation. This review also extensively covers the regulatory role of lipid metabolites such as prostaglandins and specialized pro‐resolving mediators (SPMs) that are synthesized from polyunsaturated fatty acids. Notably, SPM biosynthesis is impaired in obesity and contributes toward impaired antibody production. Future directions for research, including avenues for therapeutic intervention, are included.

中文翻译：

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荷尔蒙失调和不平衡的专门促分解介质生物合成会导致肥胖 B 细胞结果受损。

饮食引起的肥胖与 B 细胞驱动的体液免疫受损有关，这与慢性炎症同时发生，并对感染和疫苗接种的反应产生影响。综述了肥胖可能损害体液免疫各个方面的关键营养、细胞和分子机制，例如 B 细胞发育、类别转换重组和长寿命抗体分泌细胞的形成。出现的一个关键主题是白色脂肪组织对促炎 B 细胞亚群的形成和功能的核心作用，而促炎 B 细胞亚群会加剧胰岛素抵抗。强调了瘦素等特定激素的潜在作用，它可能在没有抗原刺激的情况下驱动促炎 B 细胞的形成。这篇综述还广泛涵盖了脂质代谢物的调节作用，例如前列腺素和由多不饱和脂肪酸合成的专门促分解介质（SPM）。值得注意的是，SPM 生物合成在肥胖症中受损，并导致抗体产生受损。其中包括未来的研究方向，包括治疗干预的途径。