Effector CD4 T cells with progenitor potential mediate chronic intestinal inflammation.
Boyoung ShinRobert L KressPhilip A KramerVictor M Darley-UsmarSusan L BellisLaurie E HarringtonPublished in: The Journal of experimental medicine (2018)
Dysregulated CD4 T cell responses are causally linked to autoimmune and chronic inflammatory disorders, yet the cellular attributes responsible for maintaining the disease remain poorly understood. Herein, we identify a discrete population of effector CD4 T cells that is able to both sustain and confer intestinal inflammation. This subset of pathogenic CD4 T cells possesses a unique gene signature consistent with self-renewing T cells and hematopoietic progenitor cells, exhibits enhanced survival, and continually seeds the terminally differentiated IFNγ-producing cells in the inflamed intestine. Mechanistically, this population selectively expresses the glycosyltransferase ST6Gal-I, which is required for optimal expression of the stemness-associated molecule TCF1 by effector CD4 T cells. Our findings indicate that the chronicity of T cell-mediated inflammation is perpetuated by specific effector CD4 T cells with stem-like properties.
Keyphrases
- oxidative stress
- dendritic cells
- regulatory t cells
- type iii
- induced apoptosis
- stem cells
- poor prognosis
- immune response
- bone marrow
- drug induced
- epithelial mesenchymal transition
- cell cycle arrest
- genome wide
- cell proliferation
- cell death
- long non coding rna
- binding protein
- transcription factor
- climate change
- dna methylation
- genome wide identification