Source:http://linkedlifedata.com/resource/pubmed/id/15016077
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
5
|
| pubmed:dateCreated |
2004-3-12
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| pubmed:abstractText |
Protective autoimmunity was only recently recognized as a mechanism for attenuating the progression of neurodegeneration. Using a rat model of optic nerve crush or contusive spinal cord injury, and a mouse model of neurodegenerative conditions caused by injection of a toxic dose of intraocular glutamate, we show that a single low dose of whole-body or lymphoid-organ gamma-irradiation significantly improved the spontaneous recovery. Animals with severe immune deficiency or deprived of mature T cells were unable to benefit from this treatment, suggesting that the irradiation-induced neuroprotection is immune mediated. This suggestion received further support from the findings that irradiation was accompanied by an increased incidence of activated T cells in the lymphoid organs and peripheral blood and an increase in mRNA encoding for the pro-inflammatory cytokines interleukin-12 and interferon-gamma, and that after irradiation, passive transfer of a subpopulation of suppressive T cells (naturally occurring regulatory CD4(+)CD25(+) T cells) wiped out the irradiation-induced protection. These results suggest that homeostasis-driven proliferation of T cells, induced by a single low-dose irradiation, leads to boosting of T cell-mediated neuroprotection and can be utilized clinically to fight off neurodegeneration and the threat of other diseases in which defense against toxic self-compounds is needed.
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| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Mar
|
| pubmed:issn |
0953-816X
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:volume |
19
|
| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
1191-8
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:15016077-Animals,
pubmed-meshheading:15016077-Cell Division,
pubmed-meshheading:15016077-Cell Survival,
pubmed-meshheading:15016077-Central Nervous System,
pubmed-meshheading:15016077-Dose-Response Relationship, Radiation,
pubmed-meshheading:15016077-Female,
pubmed-meshheading:15016077-Gamma Rays,
pubmed-meshheading:15016077-Homeostasis,
pubmed-meshheading:15016077-Mice,
pubmed-meshheading:15016077-Mice, Inbred BALB C,
pubmed-meshheading:15016077-Mice, Inbred C57BL,
pubmed-meshheading:15016077-Mice, SCID,
pubmed-meshheading:15016077-Neurons,
pubmed-meshheading:15016077-Optic Nerve Injuries,
pubmed-meshheading:15016077-Rats,
pubmed-meshheading:15016077-Rats, Inbred Lew,
pubmed-meshheading:15016077-Rats, Sprague-Dawley,
pubmed-meshheading:15016077-Retinal Ganglion Cells,
pubmed-meshheading:15016077-T-Lymphocytes
|
| pubmed:year |
2004
|
| pubmed:articleTitle |
Low-dose gamma-irradiation promotes survival of injured neurons in the central nervous system via homeostasis-driven proliferation of T cells.
|
| pubmed:affiliation |
Department of Neurobiology, The Weizmann Institute of Science, Rehovot, Israel.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
|