Suppr超能文献

产生白细胞介素-10的滤泡辅助性T细胞随年龄增长而积累,并将炎症与年龄相关的免疫抑制联系起来。

IL-10-producing Tfh cells accumulate with age and link inflammation with age-related immune suppression.

作者信息

Almanan Maha, Raynor Jana, Ogunsulire Ireti, Malyshkina Anna, Mukherjee Shibabrata, Hummel Sarah A, Ingram Jennifer T, Saini Ankur, Xie Markus M, Alenghat Theresa, Way Sing Sing, Deepe George S, Divanovic Senad, Singh Harinder, Miraldi Emily, Zajac Allan J, Dent Alexander L, Hölscher Christoph, Chougnet Claire, Hildeman David A

机构信息

Division of Immunobiology, Department of Pediatrics, Cincinnati Children's Hospital, University of Cincinnati College of Medicine, Cincinnati, OH 45229, USA.

Division of Infection Immunology, Research Center Borstel, Borstel, Germany.

出版信息

Sci Adv. 2020 Jul 29;6(31):eabb0806. doi: 10.1126/sciadv.abb0806. eCollection 2020 Jul.

Abstract

Aging results in profound immune dysfunction, resulting in the decline of vaccine responsiveness previously attributed to irreversible defects in the immune system. In addition to increased interleukin-6 (IL-6), we found aged mice exhibit increased systemic IL-10 that requires forkhead box P3-negative (FoxP3), but not FoxP3, CD4T cells. Most IL-10-producing cells manifested a T follicular helper (Tfh) phenotype and required the Tfh cytokines IL-6 and IL-21 for their accrual, so we refer to them as Tfh10 cells. IL-21 was also required to maintain normal serum levels of IL-6 and IL-10. Notably, antigen-specific Tfh10 cells arose after immunization of aged mice, and neutralization of IL-10 receptor signaling significantly restored Tfh-dependent antibody responses, whereas depletion of FoxP3 regulatory and follicular regulatory cells did not. Thus, these data demonstrate that immune suppression with age is reversible and implicate Tfh10 cells as an intriguing link between "inflammaging" and impaired immune responses with age.

摘要

衰老会导致严重的免疫功能障碍,致使先前归因于免疫系统不可逆缺陷的疫苗反应性下降。除了白细胞介素-6(IL-6)增加外,我们发现老年小鼠全身IL-10增加,这需要叉头框P3阴性(FoxP3阴性)而非FoxP3阳性的CD4 T细胞。大多数产生IL-10的细胞表现出滤泡辅助性T细胞(Tfh)表型,并且其积累需要Tfh细胞因子IL-6和IL-21,因此我们将它们称为Tfh10细胞。维持IL-6和IL-10的正常血清水平也需要IL-21。值得注意的是,老年小鼠免疫后会出现抗原特异性Tfh10细胞,中和IL-10受体信号可显著恢复Tfh依赖性抗体反应,而耗尽FoxP3调节性和滤泡调节性细胞则不然。因此,这些数据表明衰老导致的免疫抑制是可逆的,并表明Tfh10细胞是“炎症衰老”与衰老相关免疫反应受损之间的一个有趣联系。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/b04f/7439492/eb99d9c6a864/abb0806-F1.jpg

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验