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Antigen presentation by lung epithelial cells directs CD4+ TRM cell function and regulates barrier immunity.
- Source :
- Nature Communications; 10/5/2021, Vol. 12 Issue 1, p1-16, 16p
- Publication Year :
- 2021
-
Abstract
- Barrier tissues are populated by functionally plastic CD4<superscript>+</superscript> resident memory T (T<subscript>RM</subscript>) cells. Whether the barrier epithelium regulates CD4<superscript>+</superscript> T<subscript>RM</subscript> cell locations, plasticity and activities remains unclear. Here we report that lung epithelial cells, including distinct surfactant protein C (SPC)<superscript>low</superscript>MHC<superscript>high</superscript> epithelial cells, function as anatomically-segregated and temporally-dynamic antigen presenting cells. In vivo ablation of lung epithelial MHC-II results in altered localization of CD4<superscript>+</superscript> T<subscript>RM</subscript> cells. Recurrent encounters with cognate antigen in the absence of epithelial MHC-II leads CD4<superscript>+</superscript> T<subscript>RM</subscript> cells to co-express several classically antagonistic lineage-defining transcription factors, changes their cytokine profiles, and results in dysregulated barrier immunity. In addition, lung epithelial MHC-II is needed for surface expression of PD-L1, which engages its ligand PD-1 to constrain lung CD4<superscript>+</superscript> T<subscript>RM</subscript> cell phenotypes. Thus, we establish epithelial antigen presentation as a critical regulator of CD4<superscript>+</superscript> T<subscript>RM</subscript> cell function and identify epithelial-CD4<superscript>+</superscript> T<subscript>RM</subscript> cell immune interactions as core elements of barrier immunity. The maintenance of T resident memory (T<subscript>RM</subscript>) cells within pulmonary tissues is incompletely understood. Here the authors show that antigen presentation by lung epithelial cells maintains function and phenotype of pulmonary T<subscript>RM</subscript> cells within specific locational niches. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 20411723
- Volume :
- 12
- Issue :
- 1
- Database :
- Complementary Index
- Journal :
- Nature Communications
- Publication Type :
- Academic Journal
- Accession number :
- 152852734
- Full Text :
- https://doi.org/10.1038/s41467-021-26045-w