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Fibroblastic reticular cells enhance T cell metabolism and survival via epigenetic remodeling
- Source :
- Nat Immunol
- Publication Year :
- 2019
- Publisher :
- Springer Science and Business Media LLC, 2019.
-
Abstract
- Lymph node fibroblastic reticular cells (FRCs) respond to signals from activated T cells by releasing nitric oxide, which inhibits T cell proliferation and restricts the size of the expanding T cell pool. Whether interactions with FRCs also support the function or differentiation of activated CD8(+) T cells is not known. Here we report that encounters with FRCs enhanced cytokine production and remodeled chromatin accessibility in newly activated CD8(+) T cells via interleukin-6. These epigenetic changes facilitated metabolic reprogramming and amplified the activity of pro-survival pathways through differential transcription factor activity. Accordingly, FRC conditioning significantly enhanced the persistence of virus-specific CD8+ T cells in vivo and augmented their differentiation into tissue-resident memory T cells. Our study demonstrates that FRCs play a role beyond restricting T cell expansion—they can also shape the fate and function of CD8(+) T cells.
- Subjects :
- Cytotoxicity, Immunologic
0301 basic medicine
Cell Survival
Cellular differentiation
medicine.medical_treatment
T cell
Immunology
CD8-Positive T-Lymphocytes
Lymphocyte Activation
Nitric Oxide
Article
Epigenesis, Genetic
Mice
03 medical and health sciences
0302 clinical medicine
Reticular cell
medicine
Animals
Immunology and Allergy
Lymph node
Cells, Cultured
Cell Proliferation
Mice, Knockout
Interleukin-6
Cell growth
Chemistry
Cell Differentiation
Fibroblasts
Cellular Reprogramming
Chromatin Assembly and Disassembly
Chromatin
Cell biology
Mice, Inbred C57BL
030104 developmental biology
medicine.anatomical_structure
Cytokine
Gene Expression Regulation
Lymph Nodes
Immunologic Memory
CD8
030215 immunology
Subjects
Details
- ISSN :
- 15292916 and 15292908
- Volume :
- 20
- Database :
- OpenAIRE
- Journal :
- Nature Immunology
- Accession number :
- edsair.doi.dedup.....b22e7710b99828efbfd6c0eec8e85a1f