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Neuron-mediated generation of regulatory T cells from encephalitogenic T cells suppresses EAE.

Liu, Yawei LU ; Teige, Ingrid LU ; Birnir, Bryndis LU and Issazadeh, Shohreh LU (2006) In Nature Medicine 12(5). p.518-525
Abstract
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... (More)
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. (Less)
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organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Nature Medicine
volume
12
issue
5
pages
518 - 525
publisher
Nature Publishing Group
external identifiers
  • wos:000238149100035
  • pmid:16633347
  • scopus:33646596928
ISSN
1546-170X
DOI
10.1038/nm1402
language
English
LU publication?
yes
additional info
The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Neuroinflammation (013210006), Department of Clinical Sciences, Malmö (013240000), GABA Channels in Physiology and Pharmacology (013241570), Immunology (013212020)
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d63c814c-a6a2-4ba6-8b60-535b2fb6a60f (old id 155789)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=16633347&dopt=Abstract
date added to LUP
2016-04-01 16:53:42
date last changed
2022-04-07 19:27:02
@article{d63c814c-a6a2-4ba6-8b60-535b2fb6a60f,
  abstract     = {{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.}},
  author       = {{Liu, Yawei and Teige, Ingrid and Birnir, Bryndis and Issazadeh, Shohreh}},
  issn         = {{1546-170X}},
  language     = {{eng}},
  number       = {{5}},
  pages        = {{518--525}},
  publisher    = {{Nature Publishing Group}},
  series       = {{Nature Medicine}},
  title        = {{Neuron-mediated generation of regulatory T cells from encephalitogenic T cells suppresses EAE.}},
  url          = {{http://dx.doi.org/10.1038/nm1402}},
  doi          = {{10.1038/nm1402}},
  volume       = {{12}},
  year         = {{2006}},
}