Eomesodermin-expressing T-helper cells are essential for chronic neuroinflammation.

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.

journal_name

Nat Commun

journal_title

Nature communications

authors

Raveney BJ,Oki S,Hohjoh H,Nakamura M,Sato W,Murata M,Yamamura T

doi

10.1038/ncomms9437

subject

Has Abstract

pub_date

2015-10-05 00:00:00

pages

8437

issn

2041-1723

pii

ncomms9437

journal_volume

6

pub_type

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