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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
7
|
| pubmed:dateCreated |
1998-10-22
|
| pubmed:abstractText |
Experimental autoimmune encephalomyelitis (EAE) and other organ-specific autoimmune diseases are induced by autoantigen-specific Th1 cells. In contrast, transfer of autoantigen-reactive Th2 cells that produce IL-4 and IL-10 can prevent and/or reverse EAE. The relative roles of these two Th2 cytokines in the regulation of EAE has not been evaluated. Utilizing IL-4 and IL-10 knockout mice deficient for these cytokines and IL-10 and IL-4 transgenic mice overexpressing these cytokines, we demonstrate that IL-10-deficient mice (IL-10(-/-)) are more susceptible and develop a more severe EAE when compared with IL-4-deficient mice (IL-4(-/-)) or wild-type mice. T cells from IL-10(-/-) mice exhibit a stronger Ag-specific proliferation, produce more proinflammatory cytokines (IFN-gamma and TNF-alpha) when stimulated with an encephalitogenic peptide, and induce very severe EAE upon transfer into wild-type mice. In contrast, while IL-4 transgenic mice develop similar disease compared with their nontransgenic littermates, mice transgenic for IL-10 are completely resistant to the development of EAE. Taken together, our data suggest that IL-10 plays a more critical role in the regulation of EAE by regulating autopathogenic Th1 responses.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-10,
http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-4,
http://linkedlifedata.com/resource/pubmed/chemical/Myelin Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Myelin-Associated Glycoprotein,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/myelin oligodendrocyte glycoprotein
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Oct
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
161
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
3299-306
|
| pubmed:dateRevised |
2011-11-17
|
| pubmed:meshHeading |
pubmed-meshheading:9759845-Adoptive Transfer,
pubmed-meshheading:9759845-Amino Acid Sequence,
pubmed-meshheading:9759845-Animals,
pubmed-meshheading:9759845-Cell Line,
pubmed-meshheading:9759845-Cytokines,
pubmed-meshheading:9759845-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:9759845-Female,
pubmed-meshheading:9759845-Immunity, Innate,
pubmed-meshheading:9759845-Interleukin-10,
pubmed-meshheading:9759845-Interleukin-4,
pubmed-meshheading:9759845-Lymphocyte Activation,
pubmed-meshheading:9759845-Mice,
pubmed-meshheading:9759845-Mice, Inbred C57BL,
pubmed-meshheading:9759845-Mice, Knockout,
pubmed-meshheading:9759845-Mice, Transgenic,
pubmed-meshheading:9759845-Molecular Sequence Data,
pubmed-meshheading:9759845-Myelin Proteins,
pubmed-meshheading:9759845-Myelin-Associated Glycoprotein,
pubmed-meshheading:9759845-Peptides,
pubmed-meshheading:9759845-T-Lymphocytes
|
| pubmed:year |
1998
|
| pubmed:articleTitle |
IL-10 is critical in the regulation of autoimmune encephalomyelitis as demonstrated by studies of IL-10- and IL-4-deficient and transgenic mice.
|
| pubmed:affiliation |
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
|
| pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|