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组织内共刺激分子ICOS促进CD8+组织驻留记忆T细胞的建立
作者:小柯机器人 发布时间:2021/12/24 23:38:51

美国明尼苏达大学Stephen C. Jameson团队发现,组织内共刺激分子ICOS促进CD8+组织驻留记忆T细胞的建立。相关论文于2021年12月20日在线发表在《免疫》杂志上。

研究人员报道了ICOS在组织驻留记忆(Trem)细胞分化中的贡献。转移到WT小鼠体内后,Icos-/- CD8+ T细胞表现出Trem生成缺陷,但能正常产生循环记忆群。ICOS缺失或ICOS-L阻断影响了CD8+ Trm细胞的建立,但不影响其维持。在CD8T细胞诱导过程中,ICOS对接并不决定Trem的诱导;相反,效应CD8T细胞在接种到Icosl-/-小鼠体内后显示出Trem分化的减少。

IcosYF/YF CD8+ T细胞在Trim的产生方面受到影响,表明了PI3K信号的关键作用。少数Icos-/- Trm细胞中适度的转录变化表明,ICOS-PI3K信号主要增强了CD8+ T细胞组织驻留的效率。因此,局部的ICOS信号促进了Trem细胞的产生,这揭示了在组织驻留群体的产生过程中,共刺激信号的贡献。

据悉,共刺激受体Icos的基因表达升高是CD8Trem细胞的一个标志。

附:英文原文

Title: Engagement of the costimulatory molecule ICOS in tissues promotes establishment of CD8+ tissue-resident memory T cells

Author: Changwei Peng, Matthew A. Huggins, Kelsey M. Wanhainen, Todd P. Knutson, Hanbin Lu, Hristo Georgiev, Kristen L. Mittelsteadt, Nicholas N. Jarjour, Haiguang Wang, Kristin A. Hogquist, Daniel J. Campbell, Henrique Borges da Silva, Stephen C. Jameson

Issue&Volume: 2021-12-20

Abstract: Elevated gene expression of the costimulatory receptor Icos is a hallmark of CD8+ tissue-resident memory (Trm) T cells. Here, we examined the contribution of ICOSin Trm cell differentiation. Upon transfer into WT mice, Icos/ CD8+ T cells exhibited defective Trm generation but produced recirculating memory populationsnormally. ICOS deficiency or ICOS-L blockade compromised establishment of CD8+ Trm cells but not their maintenance. ICOS ligation during CD8+ T cell priming did not determine Trm induction; rather, effector CD8+ T cells showed reduced Trm differentiation after seeding into Icosl/ mice. IcosYF/YF CD8+ T cells were compromised in Trm generation, indicating a critical role for PI3K signaling.Modest transcriptional changes in the few Icos/ Trm cells suggest that ICOS-PI3K signaling primarily enhances the efficiency of CD8+ T cell tissue residency. Thus, local ICOS signaling promotes production of Trm cells,providing insight into the contribution of costimulatory signals in the generationof tissue-resident populations.

DOI: 10.1016/j.immuni.2021.11.017

Source: https://www.cell.com/immunity/fulltext/S1074-7613(21)00509-4

期刊信息

Immunity:《免疫》,创刊于1994年。隶属于细胞出版社,最新IF:21.522
官方网址:https://www.cell.com/immunity/home
投稿链接:https://www.editorialmanager.com/immunity/default.aspx