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金黄色葡萄球菌肠毒素 A 诱导的 αβT 细胞快速反应调控固有免疫。

Rapid αβ T-cell responses orchestrate innate immunity in response to Staphylococcal enterotoxin A.

机构信息

Department of Immunology, University of Connecticut Health Center, Farmington, Connecticut, USA.

出版信息

Mucosal Immunol. 2013 Sep;6(5):1006-15. doi: 10.1038/mi.2012.138. Epub 2013 Jan 16.

Abstract

In the generation of a traditional immune response against invading pathogens, innate cells guide T cells by programming their differentiation. However, here we demonstrate that αβ T cells have an essential role in priming innate immunity in the lung after Staphylococcus aureus enterotoxin A (SEA) inhalation. We found that SEA induces waves of cellular activation, cytokine production, and migration into the lung tissue and airways. However, this innate response was completely inhibited in the absence of αβ T cells. Specifically, we found that interleukin (IL)-17A was required for the recruitment of neutrophils and monocytes into the lung. The cellular source of IL-17A was γδ T cells, which increased their IL-17A production following SEA but only in an αβ T-cell-dependent manner. Thus, rapid T-cell activation orchestrates innate immunity and may be a new point of therapeutic intervention for acute lung injury.

摘要

在针对入侵病原体的传统免疫反应的产生过程中,先天细胞通过编程其分化来指导 T 细胞。然而,在这里我们证明,在金黄色葡萄球菌肠毒素 A(SEA)吸入后,αβ T 细胞在肺部固有免疫的启动中具有重要作用。我们发现,SEA 诱导细胞激活、细胞因子产生和迁移到肺组织和气道的波次。然而,在缺乏 αβ T 细胞的情况下,这种先天反应完全受到抑制。具体而言,我们发现白细胞介素(IL)-17A 是将中性粒细胞和单核细胞募集到肺部所必需的。IL-17A 的细胞来源是 γδ T 细胞,SEA 后其 IL-17A 产生增加,但仅以 αβ T 细胞依赖性方式增加。因此,快速 T 细胞激活协调固有免疫,可能是急性肺损伤的新的治疗干预点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/845a/3722268/2168346e2f83/nihms457854f1.jpg

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