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Neuron-mediated generation of regulatory T cells from encephalitogenic T cells suppresses EAE.
Institute for Experimental Medical Science, University of Lund. (Neuroinflammation Unit)ORCID iD: 0000-0002-1763-0266
2006 (English)In: Nature Medicine, ISSN 1078-8956, E-ISSN 1546-170X, Vol. 12, no 5, 518-25 p.Article in journal (Refereed) Published
Abstract [en]

Neurons have been neglected as cells with a major immune-regulatory function because they do not express major histocompatibility complex class II. Our data show that neurons are highly immune regulatory, having a crucial role in governing T-cell response and central nervous system (CNS) inflammation. Neurons induce the proliferation of activated CD4+ T cells through B7-CD28 and transforming growth factor (TGF)-beta1-TGF-beta receptor signaling pathways, resulting in amplification of T-cell receptor signaling through phosphorylated ZAP-70, interleukin (IL)-2 and IL-9. The interaction between neurons and T cells results in the conversion of encephalitogenic T cells to CD25+ TGF-beta1+ CTLA-4+ FoxP3+ T regulatory (Treg) cells that suppress encephalitogenic T cells and inhibit experimental autoimmune encephalomyelitis. Suppression is dependent on cytotoxic T lymphocyte antigen (CTLA)-4 but not TGF-beta1. Autocrine action of TGF-beta1, however, is important for the proliferative arrest of Treg cells. Blocking the B7 and TGF-beta pathways prevents the CNS-specific generation of Treg cells. These findings show that generation of neuron-dependent Treg cells in the CNS is instrumental in regulating CNS inflammation.

Place, publisher, year, edition, pages
2006. Vol. 12, no 5, 518-25 p.
National Category
Neurosciences Immunology in the medical area
Identifiers
URN: urn:nbn:se:uu:diva-182695DOI: 10.1038/nm1402PubMedID: 16633347OAI: oai:DiVA.org:uu-182695DiVA: diva2:560587
Available from: 2012-10-15 Created: 2012-10-15 Last updated: 2017-12-07

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