B cells constitute abundant cellular components in inflamed human tissues, but their role in pathogenesis of inflammatory T helper (T_H) subsets is still unclear. Here, we demonstrate that B cells, particularly resting naïve B cells, have a previously unrecognized helper function that is involved in shaping the metabolic process and subsequent inflammatory differentiation of T-cell receptor–primed T_H cells. ICOS/ICOSL axis–mediated glucose incorporation and utilization were crucial for inflammatory T_H subset induction by B cells, and activation of mTOR was critical for T cell glycolysis in this process. Consistently, upon encountering ICOSL⁺ B cells, activated effector memory T_H cells from patients with rheumatoid arthritis or systemic lupus erythematosus spontaneously differentiated into inflammatory T_H subsets. Immunotherapy using rituximab that specifically depleted B cells in patients with rheumatoid arthritis efficiently abrogated the capabilities of memory T_H cells to incorporate and use glucose, thereby impairing the pathogenic differentiation of inflammatory T_H subsets.

_{B 细胞在发炎的人体组织中构成丰富的细胞成分，但它们在炎症性 T 辅助细胞 (T H} ) 亚群发病机制中的作用仍不清楚。在这里，我们证明 B 细胞，尤其是静止的幼稚 B 细胞，具有以前未被识别的辅助功能，该功能参与塑造 T 细胞受体引发的 T _H细胞的代谢过程和随后的炎症分化。ICOS/ICOSL 轴介导的葡萄糖掺入和利用对于B 细胞诱导炎症性 T _{H亚群至关重要，而 mTOR 的激活对于该过程中的 T 细胞糖酵解至关重要。}一致地，在遇到 ICOSL ⁺ B 细胞时，激活效应记忆 T _H来自类风湿性关节炎或系统性红斑狼疮患者的细胞自发分化为炎性 T _H亚群。使用利妥昔单抗进行的免疫疗法可以特异性地消耗类风湿性关节炎患者的 B 细胞，从而有效地消除了记忆 T _H细胞吸收和利用葡萄糖的能力，从而削弱了炎症性 T _H亚群的致病分化。