pubmed-article:16172260 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:16172260 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:16172260 | lifeskim:mentions | umls-concept:C0004096 | lld:lifeskim |
pubmed-article:16172260 | lifeskim:mentions | umls-concept:C0021368 | lld:lifeskim |
pubmed-article:16172260 | lifeskim:mentions | umls-concept:C0026336 | lld:lifeskim |
pubmed-article:16172260 | lifeskim:mentions | umls-concept:C1336681 | lld:lifeskim |
pubmed-article:16172260 | lifeskim:mentions | umls-concept:C1527148 | lld:lifeskim |
pubmed-article:16172260 | pubmed:issue | 6 | lld:pubmed |
pubmed-article:16172260 | pubmed:dateCreated | 2005-9-20 | lld:pubmed |
pubmed-article:16172260 | pubmed:abstractText | Thymic stromal lymphopoietin (TSLP) is a cytokine that promotes CD4+ T cell homeostasis. We now demonstrate that TSLP is required to mount a normal CD4+ T cell-mediated inflammatory response. TSLP acts directly on naive, but not, memory CD4+ T cells, and promotes their proliferation in response to antigen. In addition, TSLP exerts an effect indirectly through DCs to promote Th2 differentiation of CD4+ T cells. Correspondingly, TSLP receptor (TSLPR) knockout (KO) mice exhibit strong Th1 responses, with high levels of interleukin (IL)-12, interferon-gamma, and immunoglobulin (Ig) G2a, but low production of IL-4, -5, -10, -13, and IgE; moreover, CD4+ T cells from these animals proliferate less well in response to antigen. Furthermore, TSLPR KO mice fail to develop an inflammatory lung response to inhaled antigen unless supplemented with wild-type CD4+ T cells. This underscores an important role for this cytokine in the development of inflammatory and/or allergic responses in vivo. | lld:pubmed |
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pubmed-article:16172260 | pubmed:language | eng | lld:pubmed |
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pubmed-article:16172260 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:16172260 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:16172260 | pubmed:month | Sep | lld:pubmed |
pubmed-article:16172260 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:16172260 | pubmed:author | pubmed-author:KellyJohnJ | lld:pubmed |
pubmed-article:16172260 | pubmed:author | pubmed-author:LeonardWarren... | lld:pubmed |
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pubmed-article:16172260 | pubmed:author | pubmed-author:SpolskiRosann... | lld:pubmed |
pubmed-article:16172260 | pubmed:author | pubmed-author:Al-ShamiAminA | lld:pubmed |
pubmed-article:16172260 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:16172260 | pubmed:day | 19 | lld:pubmed |
pubmed-article:16172260 | pubmed:volume | 202 | lld:pubmed |
pubmed-article:16172260 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:16172260 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:16172260 | pubmed:pagination | 829-39 | lld:pubmed |
pubmed-article:16172260 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:16172260 | pubmed:year | 2005 | lld:pubmed |
pubmed-article:16172260 | pubmed:articleTitle | A role for TSLP in the development of inflammation in an asthma model. | lld:pubmed |
pubmed-article:16172260 | pubmed:affiliation | Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA. | lld:pubmed |
pubmed-article:16172260 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:16172260 | pubmed:publicationType | Research Support, N.I.H., Intramural | lld:pubmed |
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