在粘膜部位形成的生发中心（GC）暴露于肠道衍生因子，这些因子有可能独立于抗原受体驱动的选择性过程影响体内平衡。 G 蛋白 Gα13 将 B 细胞限制在 GC 内，并限制 GC 衍生淋巴瘤的发展。我们发现 Gα13 缺陷通过增加 mTORC1 信号传导和 Myc 蛋白表达（特别是在肠系膜淋巴结 (mLN) 中）来促进 GC 反应。 mLN 中 Gα13 缺陷的 GC B 细胞 (GCB) 的竞争优势不依赖于 T 细胞帮助或肠道微生物群。相反，Gα13 缺陷的 GCB 选择性地依赖饮食营养素，这可能是因为更容易进入肠道淋巴管。具体来说，我们发现饮食来源的谷氨酰胺支持 mLN 中 Gα13 缺陷的 GCB 的增殖和 Myc 表达。因此，GC 限制限制了膳食谷氨酰胺对粘膜组织中 GC 动态的影响。 Gα13 通路突变会利用这些过程来促进侵袭性淋巴瘤的肠道向性。© 2024。这是美国政府的作品，在美国不受版权保护；外国版权保护可能适用。

Germinal centers (GCs) that form in mucosal sites are exposed to gut-derived factors that have the potential to influence homeostasis independent of antigen receptor-driven selective processes. The G-protein Gα13 confines B cells to the GC and limits the development of GC-derived lymphoma. We discovered that Gα13-deficiency fuels the GC reaction via increased mTORC1 signaling and Myc protein expression specifically in the mesenteric lymph node (mLN). The competitive advantage of Gα13-deficient GC B cells (GCBs) in mLN was not dependent on T cell help or gut microbiota. Instead, Gα13-deficient GCBs were selectively dependent on dietary nutrients likely due to greater access to gut lymphatics. Specifically, we found that diet-derived glutamine supported proliferation and Myc expression in Gα13-deficient GCBs in the mLN. Thus, GC confinement limits the effects of dietary glutamine on GC dynamics in mucosal tissues. Gα13 pathway mutations coopt these processes to promote the gut tropism of aggressive lymphoma.© 2024. This is a U.S. Government work and not under copyright protection in the US; foreign copyright protection may apply.