Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

. 2021 Jul 22;218(9):e20202715. doi: 10.1084/jem.20202715

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 2021 Sanmarco et al.

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/).

PMC Copyright notice

Figure 1. — Astrocyte–T cell bidirectional communication. (A) Regulatory T (Treg) cells limit astrogliosis via the production of amphiregulin and IL-10. Astrocytes express CTLA-4, CD73, and CD39, leading to T cell suppression. LAMP1⁺TRAIL⁺ astrocytes induce apoptosis of DR5⁺ T cells. (B) Astrocyte–T cell interactions via integrins can boost CNS inflammation. Astrocytes release pro-inflammatory cytokines to recruit and polarize pathogenic T cells. Th17 cells induce astrogliosis and VEGF up-regulation, whereas Th1 cells increase MHC class II and costimulation. GM-CSF activates MAFG-driven pathogenic activities in astrocytes.