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

. 2023 Apr 17;20(1):9–19. doi: 10.1007/s11302-023-09939-w

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

© The Author(s) 2023

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

PMC Copyright notice

Fig. 1 — P2X7R mediated control of tissue resident effector T cells and Th17 polarization in the intestine. Luminal eATP is hypothesized to reach the intestinal lamina propria through Paneth cells, tight junctions or trancytosis by M cells. In P2xr7^+/+ mice, RA promotes P2rx7 transcription via binding of RAR complex to an intragenic enhancer region of P2rx7 in CD8, CD4 T and iNKT cell. P2rx7 upregulation renders these cell populations susceptible to P2X7R-mediated cell death, contributing to the regulation of T effector/memory and iNKT cells in the intestine. An eATP/P2XR axis can activate CD70 CD11 DCs, promoting Th17 polarization from naïve T cells. P2X7R signaling promotes Treg cell conversion to Th17 and also cell death, thereby further decreasing Treg cell number. In P2rx7^-/- mice, lack of P2X7R activity results in increased CD8 T cell response to Listeria monocytogenes. P2X7R deletion in Treg cell is associated with enhanced immunosuppression and protection from chemically induced IBD. Created with BioRender