Eomesodermin-expressing T-helper cells are essential for chronic neuroinflammation.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 26436530.
- Also identified by DOI 10.1038/ncomms9437 and PMC identifier 4600741.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Development of acute experimental autoimmune encephalomyelitis (EAE) depends on Th17 cells expressing the nuclear factor NR4A2. However, in mice lacking NR4A2 in T cells, a late-onset disease is still inducible, despite a great reduction in acute inflammation. We here reveal that development of this late onset disease depends on cytotoxic T-cell-like CD4(+) T cells expressing the T-box transcription factor Eomesodermin (Eomes). T-cell-specific deletion of the Eomes gene remarkably ameliorates the late-onset EAE. Strikingly, similar Eomes(+) CD4(+) T cells are increased in the peripheral blood and cerebrospinal fluid from patients in a progressive state of multiple sclerosis. Collective data indicate an involvement of granzyme B and protease-activated receptor-1 in the neuroinflammation mediated by Eomes(+) CD4(+) T cells.
Medical subject headings
- Encephalomyelitis, Autoimmune, Experimental
- Granzymes
- Multiple Sclerosis, Chronic Progressive
- Receptor, PAR-1
- T-Box Domain Proteins
- Th17 Cells