| pubmed-article:9120387 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:9120387 | lifeskim:mentions | umls-concept:C0330390 | lld:lifeskim |
| pubmed-article:9120387 | lifeskim:mentions | umls-concept:C0242633 | lld:lifeskim |
| pubmed-article:9120387 | lifeskim:mentions | umls-concept:C0021764 | lld:lifeskim |
| pubmed-article:9120387 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
| pubmed-article:9120387 | lifeskim:mentions | umls-concept:C1423842 | lld:lifeskim |
| pubmed-article:9120387 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:9120387 | lifeskim:mentions | umls-concept:C1711351 | lld:lifeskim |
| pubmed-article:9120387 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
| pubmed-article:9120387 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:9120387 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:9120387 | pubmed:dateCreated | 1997-4-21 | lld:pubmed |
| pubmed-article:9120387 | pubmed:abstractText | The developmental commitment to a T helper 1 (Th1)- or Th2-type response can significantly influence host immunity to pathogens. Extinction of the IL-12 signaling pathway during early Th2 development provides a mechanism that allows stable phenotype commitment. In this report we demonstrate that extinction of IL-12 signaling in early Th2 cells results from a selective loss of IL-12 receptor (IL-12R) beta 2 subunit expression. To determine the basis for this selective loss, we examined IL-12R beta 2 subunit expression during Th cell development in response to T cell treatment with different cytokines. IL-12R beta 2 is not expressed by naive resting CD4+ T cells, but is induced upon antigen activation through the T cell receptor. Importantly, IL-4 and IFN-gamma were found to significantly modify IL-12 receptor beta 2 expression after T cell activation. IL-4 inhibited IL-12R beta 2 expression leading to the loss of IL-12 signaling, providing an important point of regulation to promote commitment to the Th2 pathway. IFN-gamma treatment of early developing Th2 cells maintained IL-12R beta 2 expression and restored the ability of these cells to functionally respond to IL-12, but did not directly inhibit IL-4 or induce IFN-gamma production. Thus, IFN-gamma may prevent early Th cells from premature commitment to the Th2 pathway. Controlling the expression of the IL-12R beta 2 subunit could be an important therapeutic target for the redirection of ongoing Th cell responses. | lld:pubmed |
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| pubmed-article:9120387 | pubmed:language | eng | lld:pubmed |
| pubmed-article:9120387 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:9120387 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:9120387 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:9120387 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:9120387 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:9120387 | pubmed:issn | 0022-1007 | lld:pubmed |
| pubmed-article:9120387 | pubmed:author | pubmed-author:GublerUU | lld:pubmed |
| pubmed-article:9120387 | pubmed:author | pubmed-author:MurphyK MKM | lld:pubmed |
| pubmed-article:9120387 | pubmed:author | pubmed-author:SzaboS JSJ | lld:pubmed |
| pubmed-article:9120387 | pubmed:author | pubmed-author:DigheA SAS | lld:pubmed |
| pubmed-article:9120387 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:9120387 | pubmed:day | 3 | lld:pubmed |
| pubmed-article:9120387 | pubmed:volume | 185 | lld:pubmed |
| pubmed-article:9120387 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:9120387 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:9120387 | pubmed:pagination | 817-24 | lld:pubmed |
| pubmed-article:9120387 | pubmed:dateRevised | 2009-11-19 | lld:pubmed |
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