Source:http://linkedlifedata.com/resource/pubmed/id/19966187
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2009-12-23
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pubmed:abstractText |
Besides being mandatory in the metabolic system, adipokines like leptin directly affect immunity. Leptin was found to be necessary in T helper 1 (Th1)-dependent inflammatory processes, whereas effects on Th2 cells are rarely understood. Here, we focused on leptin in T-helper cell polarization and in Th2-mediated intestinal inflammation in vivo. The induction of cytokine-producing Th1 or Th2 cells from naive CD4(+) T cells under polarizing conditions in vitro was generally decreased in cells from leptin-deficient ob/ob mice compared with wild-type mice. To explore the in vivo relevance of leptin in Th2-mediated inflammation, the model of oxazolone-induced colitis was employed in wild-type, ob/ob, and leptin-reconstituted ob/ob mice. Ob/ob mice were protected, whereas wild-type and leptin-reconstituted ob/ob mice developed colitis. The disease severity went in parallel with local production of the Th2 cytokine IL-13. A possible explanation for the protection of ob/ob mice in Th1- as well as in Th2-dependent inflammation is provided by a decreased expression of the key transcription factors for Th1 and Th2 polarization, T-bet and GATA-3, in naive ob/ob T cells. In conclusion, these results support the regulatory function of the adipokine leptin within T-cell polarization and thus in the acquired immune system and support the concept that there is a close interaction with the endocrine system.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/GATA3 Transcription Factor,
http://linkedlifedata.com/resource/pubmed/chemical/Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/T-Box Domain Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/T-box transcription factor TBX21
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1945-7170
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:volume |
151
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
56-62
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pubmed:meshHeading |
pubmed-meshheading:19966187-Animals,
pubmed-meshheading:19966187-Apoptosis,
pubmed-meshheading:19966187-CD4-Positive T-Lymphocytes,
pubmed-meshheading:19966187-Cell Polarity,
pubmed-meshheading:19966187-Cell Proliferation,
pubmed-meshheading:19966187-Cells, Cultured,
pubmed-meshheading:19966187-Female,
pubmed-meshheading:19966187-GATA3 Transcription Factor,
pubmed-meshheading:19966187-Gastroenteritis,
pubmed-meshheading:19966187-Gene Expression Regulation,
pubmed-meshheading:19966187-Leptin,
pubmed-meshheading:19966187-Mice,
pubmed-meshheading:19966187-Mice, Inbred BALB C,
pubmed-meshheading:19966187-Mice, Inbred C57BL,
pubmed-meshheading:19966187-Mice, Obese,
pubmed-meshheading:19966187-Receptors, Leptin,
pubmed-meshheading:19966187-T-Box Domain Proteins
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pubmed:year |
2010
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pubmed:articleTitle |
Leptin: a critical regulator of CD4+ T-cell polarization in vitro and in vivo.
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pubmed:affiliation |
Charité Universitätsmedizin Berlin, Campus Benjamin Franklin, Gastroenterology, 12200 Berlin, Germany.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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