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GL7 配体表达定义了肺炎球菌感染后肺部恢复的 CD4 T 细胞的一个新亚群。

GL7 ligand expression defines a novel subset of CD4 T cells in lungs recovered from pneumococcus.

机构信息

Pulmonary Center, Boston University Chobanian & Avedesian School of Medicine, Boston, Massachusetts, USA; Department of Virology, Immunology, & Microbiology, Boston University Chobanian & Avedesian School of Medicine, Boston, Massachusetts, USA.

Pulmonary Center, Boston University Chobanian & Avedesian School of Medicine, Boston, Massachusetts, USA; Department. of Microbiology and Immunology, University of Michigan Medical School, Ann Arbor, Michigan, USA.

出版信息

Mucosal Immunol. 2023 Oct;16(5):699-710. doi: 10.1016/j.mucimm.2023.07.004. Epub 2023 Sep 14.

Abstract

Streptococcus pneumoniae is the most common etiology of bacterial pneumonia, one of the leading causes of death in children and the elderly worldwide. During non-lethal infections with S. pneumoniae, lymphocytes accumulate in the lungs and protect against reinfection with serotype-mismatched strains. Cluster of differentiation CD4 resident memory T (T) cells are known to be crucial for this protection, but the diversity of lung CD4 T cells has yet to be fully delineated. We aimed to identify unique subsets and their contributions to lung immunity. After recovery from pneumococcal infections, we identified a distinct subset of CD4 T cells defined by the phenotype CD11aCD69GL7 in mouse lungs. Phenotypic analyses for markers of lymphocyte memory and residence demonstrated that GL7 T cells are a subset of CD4 T cells. Functional studies revealed that unlike GL7 T subsets that were mostly (RAR-related Orphan Receptor gamma T) RORγT, GL7 T cells exhibited higher levels of (T-box expressed in T cells) T-bet and Gata-3, corresponding with increased synthesis of interferon-γ, interleukin-13, and interleukin-5, inherent to both T helper 1 (T1) and T2 functions. Thus, we propose that these cells provide novel contributions during pneumococcal pneumonia, serving as important determinants of lung immunity.

摘要

肺炎链球菌是细菌性肺炎最常见的病因,也是全球儿童和老年人死亡的主要原因之一。在非致死性肺炎链球菌感染中,淋巴细胞在肺部积聚,可防止与血清型不同的菌株再次感染。已知分化群 CD4 驻留记忆 T(T)细胞对于这种保护至关重要,但肺部 CD4 T 细胞的多样性尚未完全描绘。我们旨在确定独特的亚群及其对肺部免疫的贡献。在从肺炎球菌感染中恢复后,我们在小鼠肺部确定了一种独特的 CD4 T 细胞亚群,其表型为 CD11aCD69GL7。用于淋巴细胞记忆和驻留标记的表型分析表明,GL7 T 细胞是 CD4 T 细胞的一个亚群。功能研究表明,与主要为(RAR 相关孤儿受体 γ T)RORγT 的 GL7 T 亚群不同,GL7 T 细胞表现出更高水平的(T 细胞中表达的 T 框)T-bet 和 Gata-3,对应于干扰素-γ、白细胞介素-13 和白细胞介素-5 的合成增加,这与 T 辅助 1(T1)和 T2 功能都有关。因此,我们提出这些细胞在肺炎球菌性肺炎中提供新的贡献,是肺部免疫的重要决定因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a5f0/10591822/f39721925a12/nihms-1937089-f0001.jpg

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