本期文章：《细胞—代谢》：Online/在线发表

美国犹他州卫生局微生物学、免疫学和分子遗传学系Elizabeth A. Leadbetter团队近期取得重要工作进展，他们研究发现T-bet⁺ B细胞在脂肪组织中聚集并加剧了肥胖期间的代谢紊乱。相关论文2022年7月21日在线出版于《细胞—代谢》杂志上。

肥胖伴随着脂肪组织的炎症、葡萄糖耐量降低和脂肪白细胞数量的变化。 这些对人类和小鼠脂肪组织的研究表明，脂肪组织中T-bet⁺ B细胞频率的增加取决于不变的NKT细胞，并且与肥胖期间的体重增加相关。转移富含T-bet⁺细胞的B细胞会加剧肥胖症的代谢紊乱，而B细胞中特异性Tbx21的消融会降低脂肪组织中的血清IgG2c水平、炎性细胞因子和炎性巨噬细胞，从而改善代谢症状。

此外，从HFD小鼠转移血清或纯化的IgG可恢复T-bet⁺ B细胞缺陷小鼠的代谢疾病，证实T-bet⁺ B细胞衍生的IgG是肥胖期间炎症的关键介质。总之，这些发现揭示了T-bet⁺ B细胞的重要病理作用，应该为未来2型糖尿病和其他炎症性疾病的免疫治疗设计提供信息。

附：英文原文

Title: T-bet+ B cells accumulate in adipose tissue and exacerbate metabolic disorder during obesity

Author: Thomas Hgglf, Carlo Vanz, Abigail Kumagai, Elizabeth Dudley, Vanessa Ortega, McKenzie Siller, Raksha Parthasarathy, Josh Keegan, Abigail Koenigs, Travis Shute, Elizabeth A. Leadbetter

Issue&Volume: 2022-07-21

Abstract: Obesity is accompanied by inflammation in adipose tissue, impaired glucose tolerance,and changes in adipose leukocyte populations. These studies of adipose tissue fromhumans and mice revealed that increased frequencies of T-bet+ B cells in adipose tissue depend on invariant NKT cells and correlate with weightgain during obesity. Transfer of B cells enriched for T-bet+ cells exacerbates metabolic disorder in obesity, while ablation of Tbx21 specifically in B cells reduces serum IgG2c levels, inflammatory cytokines, and inflammatorymacrophages in adipose tissue, ameliorating metabolic symptoms. Furthermore, transferof serum or purified IgG from HFD mice restores metabolic disease in T-bet+ B cell-deficient mice, confirming T-bet+ B cell-derived IgG as a key mediator of inflammation during obesity. Together, thesefindings reveal an important pathological role for T-bet+ B cells that should inform future immunotherapy design in type 2 diabetes and otherinflammatory conditions.

DOI: 10.1016/j.cmet.2022.07.002