Source:http://linkedlifedata.com/resource/pubmed/id/12218142
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
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umls-concept:C1706203,
umls-concept:C1706817,
umls-concept:C2349001,
umls-concept:C2587213,
umls-concept:C2697811,
umls-concept:C2911692
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| pubmed:issue |
6
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| pubmed:dateCreated |
2002-9-9
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| pubmed:abstractText |
Susceptibility and development of Th2 cells in BALB/c mice infected with Leishmania major result from early IL-4 production by Vbeta4Valpha8 CD4+ T cells in response to the Leishmania homolog of mammalian RACK1 Ag. A role for CD4+CD25+ regulatory T cells in the control of this early IL-4 production was investigated by depleting in vivo this regulatory T cell population. Depletion induced an increase in the early burst of IL-4 mRNA in the draining lymph nodes of BALB/c mice, and exacerbated the course of disease with higher levels of IL-4 mRNA and protein in their lymph nodes. We further showed that transfer of 10(7) BALB/c spleen cells that were depleted of CD4+CD25+ regulatory T cells rendered SCID mice susceptible to infection and allowed Th2 differentiation while SCID mice reconstituted with 10(7) control BALB/c spleen cells were resistant to infection with L. major and developed a Th1 response. Treatment with a mAb against IL-4 upon infection with L. major in SCID mice reconstituted with CD25-depleted spleen cells prevented the development of Th2 polarization and rendered them resistant to infection. These results demonstrate that CD4+CD25+ regulatory T cells play a role in regulating the early IL-4 mRNA and the subsequent development of a Th2 response in this model of infection.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Sep
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| pubmed:issn |
0022-1767
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| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
15
|
| pubmed:volume |
169
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
3232-41
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| pubmed:dateRevised |
2006-11-15
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| pubmed:meshHeading |
pubmed-meshheading:12218142-Adoptive Transfer,
pubmed-meshheading:12218142-Animals,
pubmed-meshheading:12218142-Antibodies, Monoclonal,
pubmed-meshheading:12218142-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12218142-Cell Differentiation,
pubmed-meshheading:12218142-Disease Progression,
pubmed-meshheading:12218142-Disease Susceptibility,
pubmed-meshheading:12218142-Female,
pubmed-meshheading:12218142-Interleukin-4,
pubmed-meshheading:12218142-Leishmania major,
pubmed-meshheading:12218142-Leishmaniasis, Cutaneous,
pubmed-meshheading:12218142-Lymphocyte Activation,
pubmed-meshheading:12218142-Lymphocyte Depletion,
pubmed-meshheading:12218142-Mice,
pubmed-meshheading:12218142-Mice, Inbred BALB C,
pubmed-meshheading:12218142-Mice, Inbred C57BL,
pubmed-meshheading:12218142-Mice, SCID,
pubmed-meshheading:12218142-Receptors, Interleukin-2,
pubmed-meshheading:12218142-Spleen,
pubmed-meshheading:12218142-T-Lymphocyte Subsets,
pubmed-meshheading:12218142-T-Lymphocytes, Regulatory,
pubmed-meshheading:12218142-Th2 Cells
|
| pubmed:year |
2002
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| pubmed:articleTitle |
The early IL-4 response to Leishmania major and the resulting Th2 cell maturation steering progressive disease in BALB/c mice are subject to the control of regulatory CD4+CD25+ T cells.
|
| pubmed:affiliation |
World Health Organization Immunology Research and Training Center, Institute of Biochemistry, University of Lausanne, Epalinges, Switzerland.
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| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|