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

Ben J. E. Raveney, Shinji Oki, Hirohiko Hohjoh, Masakazu Nakamura, Wakiro Sato, Miho Murata and Takashi Yamamura ()
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Ben J. E. Raveney: National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-Higashi,Kodaira, Tokyo 187-8502, Japan
Shinji Oki: National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-Higashi,Kodaira, Tokyo 187-8502, Japan
Hirohiko Hohjoh: National Institute of Neuroscience, National Center of Neurology and Psychiatry, Tokyo 187-8502, Japan
Masakazu Nakamura: National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-Higashi,Kodaira, Tokyo 187-8502, Japan
Wakiro Sato: National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-Higashi,Kodaira, Tokyo 187-8502, Japan
Miho Murata: National Center Hospital, National Center of Neurology and Psychiatry, Tokyo 187-8502, Japan
Takashi Yamamura: National Institute of Neuroscience, National Center of Neurology and Psychiatry, 4-1-1 Ogawa-Higashi,Kodaira, Tokyo 187-8502, Japan

Nature Communications, 2015, vol. 6, issue 1, 1-11

Abstract: 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.

Date: 2015
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DOI: 10.1038/ncomms9437

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