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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
6052
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pubmed:dateCreated |
2011-10-7
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pubmed:abstractText |
Neural circuits regulate cytokine production to prevent potentially damaging inflammation. A prototypical vagus nerve circuit, the inflammatory reflex, inhibits tumor necrosis factor-? production in spleen by a mechanism requiring acetylcholine signaling through the ?7 nicotinic acetylcholine receptor expressed on cytokine-producing macrophages. Nerve fibers in spleen lack the enzymatic machinery necessary for acetylcholine production; therefore, how does this neural circuit terminate in cholinergic signaling? We identified an acetylcholine-producing, memory phenotype T cell population in mice that is integral to the inflammatory reflex. These acetylcholine-producing T cells are required for inhibition of cytokine production by vagus nerve stimulation. Thus, action potentials originating in the vagus nerve regulate T cells, which in turn produce the neurotransmitter, acetylcholine, required to control innate immune responses.
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pubmed:commentsCorrections |
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Oct
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pubmed:issn |
1095-9203
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pubmed:author |
pubmed-author:AnderssonUlfU,
pubmed-author:ChavanSangeetaS,
pubmed-author:LevineYaakov AYA,
pubmed-author:MakTak WTW,
pubmed-author:OchaniMahendarM,
pubmed-author:OlofssonPeder SPS,
pubmed-author:PavlovValentin AVA,
pubmed-author:ReardonColinC,
pubmed-author:Rosas-BallinaMauricioM,
pubmed-author:TraceyKevin JKJ,
pubmed-author:TuscheMichael WMW,
pubmed-author:Valdés-FerrerSergio ISI
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pubmed:issnType |
Electronic
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pubmed:day |
7
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pubmed:volume |
334
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
98-101
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pubmed:meshHeading |
pubmed-meshheading:21921156-Acetylcholine,
pubmed-meshheading:21921156-Action Potentials,
pubmed-meshheading:21921156-Animals,
pubmed-meshheading:21921156-CD4-Positive T-Lymphocytes,
pubmed-meshheading:21921156-Choline O-Acetyltransferase,
pubmed-meshheading:21921156-Cholinergic Agents,
pubmed-meshheading:21921156-Female,
pubmed-meshheading:21921156-Immunity, Innate,
pubmed-meshheading:21921156-Immunologic Memory,
pubmed-meshheading:21921156-Inflammation,
pubmed-meshheading:21921156-Lymphocyte Activation,
pubmed-meshheading:21921156-Male,
pubmed-meshheading:21921156-Mice,
pubmed-meshheading:21921156-Mice, Inbred BALB C,
pubmed-meshheading:21921156-Mice, Nude,
pubmed-meshheading:21921156-Neuroimmunomodulation,
pubmed-meshheading:21921156-Norepinephrine,
pubmed-meshheading:21921156-Receptors, Nicotinic,
pubmed-meshheading:21921156-Signal Transduction,
pubmed-meshheading:21921156-Spleen,
pubmed-meshheading:21921156-T-Lymphocyte Subsets,
pubmed-meshheading:21921156-Tumor Necrosis Factor-alpha,
pubmed-meshheading:21921156-Vagus Nerve,
pubmed-meshheading:21921156-Vagus Nerve Stimulation
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pubmed:year |
2011
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pubmed:articleTitle |
Acetylcholine-synthesizing T cells relay neural signals in a vagus nerve circuit.
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pubmed:affiliation |
Laboratory of Biomedical Science, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, New York 11030, USA.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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