Regulatory T cells (T regs ) control adaptive immunity and restrain type 2 inflammation in allergic disease. Interleukin-33 promotes the expansion of tissue-resident T regs and group 2 innate lymphoid cells (ILC2s); however, how T regs locally coordinate their function within the inflammatory niche is not understood. Here, we show that ILC2s are critical orchestrators of T reg function. Using spatial, cellular, and molecular profiling of the type 2 inflamed niche, we found that ILC2s and T regs engage in a direct (OX40L-OX40) and chemotaxis-dependent (CCL1-CCR8) cellular dialogue that enforces the local accumulation of Gata3 high T regs , which are transcriptionally and functionally adapted to the type 2 environment. Genetic interruption of ILC2-T reg communication resulted in uncontrolled type 2 lung inflammation after allergen exposure. Mechanistically, we found that Gata3 high T regs can modulate the local bioavailability of the costimulatory molecule OX40L, which subsequently controlled effector memory T helper 2 cell numbers. Hence, ILC2-T reg interactions represent a critical feedback mechanism to control adaptive type 2 immunity.

中文翻译：

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ILC2 和 Gata3 高 T 调节细胞之间的串扰局部限制适应性 2 型免疫


调节性 T 细胞（T规则）控制适应性免疫并抑制过敏性疾病中的2型炎症。 Interleukin-33 促进组织驻留 T 细胞的扩增规则和第 2 组先天淋巴细胞 (ILC2)；然而，如何T规则局部协调它们在炎症生态位内的功能尚不清楚。在这里，我们表明 ILC2 是 T 的关键协调者注册功能。利用 2 型发炎生态位的空间、细胞和分子分析，我们发现 ILC2 和 T规则参与直接 (OX40L-OX40) 和趋化依赖性 (CCL1-CCR8) 细胞对话，强制 Gata3 局部积累高的时间规则，它们在转录和功能上都适应了 2 型环境。 ILC2-T 的基因中断注册接触过敏原后，沟通会导致不受控制的 2 型肺部炎症。从机制上来说，我们发现Gata3高的时间规则可以调节共刺激分子 OX40L 的局部生物利用度，从而控制效应记忆 T 辅助细胞 2 细胞的数量。因此，ILC2-T注册相互作用是控制适应性 2 型免疫的关键反馈机制。