The exact relationships between group 2 innate lymphoid cells (ILC2s) and Th2 cells in type 2 pathology, as well as the mechanisms that restrain the responses of these cells, remain poorly defined. Here we examined the roles of ILC2s and Th2 cells in type 2 lung pathology in vivo using germline and conditional Relb-deficient mice. We found that mice with germline deletion of Relb (Relb^−/−) spontaneously developed prominent type 2 pathology in the lung, which contrasted sharply with mice with T-cell-specific Relb deletion (Relb^f/fCd4-Cre), which were healthy with no observed autoimmune pathology. We also found that in contrast to wild-type B6 mice, Relb-deficient mice showed markedly expanded ILC2s but not ILC1s or ILC3s. Moreover, adoptive transfer of naive CD4⁺ T cells into Rag1^−/−Relb^−/− hosts induced prominent type 2 lung pathology, which was inhibited by depletion of ILC2s. Mechanistically, we showed that Relb deletion led to enhanced expression of Bcl11b, a key transcription factor for ILC2s. We concluded that RelB plays a critical role in restraining ILC2s, primarily by suppressing Bcl11b activity, and consequently inhibits type 2 lung pathology in vivo.

2 型病理学中第 2 组先天淋巴细胞 (ILC2) 和 Th2 细胞之间的确切关系，以及抑制这些细胞反应的机制，仍然不清楚。在这里，我们使用生殖系和条件性Relb 缺陷小鼠检查了 ILC2s 和 Th2 细胞在体内 2 型肺病理学中的作用。我们发现具有Relb ( Relb ^-/- )种系缺失的小鼠在肺中自发地发展出显着的 2 型病理，这与具有 T 细胞特异性Relb缺失 ( Relb ^f/f Cd4-Cre ) 的小鼠形成鲜明对比。健康，没有观察到自身免疫病理。我们还发现，与野生型 B6 小鼠相比，Relb-缺陷小鼠表现出显着扩大的 ILC2s，但没有 ILC1s 或 ILC3s。此外，将幼稚 CD4 ⁺ T 细胞过继转移到Rag1 ^-/- Relb ^-/-宿主中诱导了显着的 2 型肺病理，这被 ILC2 的消耗所抑制。从机制上讲，我们发现Relb缺失导致 Bcl11b 的表达增强，Bcl11b 是 ILC2 的关键转录因子。我们得出结论，RelB 在抑制 ILC2s 中起关键作用，主要是通过抑制 Bcl11b 活性，从而在体内抑制 2 型肺病理。