Obesity is accompanied by inflammation in adipose tissue, impaired glucose tolerance, and changes in adipose leukocyte populations. These studies of adipose tissue from humans and mice revealed that increased frequencies of T-bet⁺ B cells in adipose tissue depend on invariant NKT cells and correlate with weight gain 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 inflammatory macrophages in adipose tissue, ameliorating metabolic symptoms. Furthermore, transfer of 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, these findings reveal an important pathological role for T-bet⁺ B cells that should inform future immunotherapy design in type 2 diabetes and other inflammatory conditions.

肥胖伴随着脂肪组织炎症、糖耐量受损和脂肪白细胞群的变化。^{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。富含 T-bet ⁺细胞的 B 细胞的转移会加剧肥胖的代谢紊乱，而B 细胞中特异的Tbx21消除会降低脂肪组织中的血清 IgG2c 水平、炎症细胞因子和炎症巨噬细胞，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，可为未来 2 型糖尿病和其他炎症性疾病的免疫治疗设计提供信息。