先天性淋巴细胞
胸腺基质淋巴细胞生成素
细胞因子
生物
免疫系统
免疫学
受体
先天免疫系统
生物化学
作者
Banu Batyrova,Fien Luwaert,Panagiota Maravelia,Yuria Miyabayashi,Neha Vashist,Julian M. Stark,Sara Y. Soori,Christopher A. Tibbitt,Peggy Riese,Jonathan M. Coquet,Benedict J. Chambers
摘要
Abstract Introduction Innate lymphoid cells (ILCs) can provide early cytokine help against a variety of pathogens in the lungs and gastrointestinal tract. Type 2 ILC (ILC2) are comparable to T helper 2 cells found in the adaptive immune system, which secrete cytokines such as interleukin 5 (IL‐5) and IL‐13 and have been found to play roles in host defense against helminth infections and in allergic responses. Recent studies have identified that programmed cell death protein 1 (PD‐1) and peroxisome proliferator activated receptor‐γ (PPAR‐γ) are highly expressed by ILC2. We examined whether PD‐1 plays a role in ILC2 function and whether there was any connection between PD‐1 and PPAR‐γ Methods To ensure that only innate immune cells were present, ILC2 cells were examined from RAG1 −/− and PD‐1 −/− xRAG1 −/− mice under steady‐state or following inoculation with IL‐33. We also tested ILC2 generated from bone marrow of RAG1 −/− and PD‐1 −/− xRAG1 −/− mice for their production of cytokines. These in vitro‐derived ILC2 were also exposed to agonist and antagonist of PPAR‐γ. Results We found that ILC2 from PD‐1 −/− xRAG1 −/− mice had reduced frequencies of IL‐5 and IL‐13 producing cells both in vitro upon IL‐33 stimulation and in vivo following intraperitoneal administration of IL‐33 when compared with ILC2 from RAG1 −/− mice. However, by adding IL‐2, IL‐25, and thymic stromal lymphopoietin to the in vitro cultures, the frequency of IL‐5 and IL‐13 expressing ILC2 from PD‐1 −/− xRAG1 −/− mice became similar to the frequency observed for ILC2 from RAG1 −/− mice. In addition, PPAR‐γ agonists and antagonists were found to increase and decrease PD‐1 expression on ILC2 respectively. Conclusions These findings illustrate that chronic loss of PD‐1 plays a role in ILC2 function and PD‐1 expression can be modulated by PPAR‐γ.
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