pubmed-article:12757612 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12757612 | lifeskim:mentions | umls-concept:C0034790 | lld:lifeskim |
pubmed-article:12757612 | lifeskim:mentions | umls-concept:C0004368 | lld:lifeskim |
pubmed-article:12757612 | lifeskim:mentions | umls-concept:C0439662 | lld:lifeskim |
pubmed-article:12757612 | lifeskim:mentions | umls-concept:C0686907 | lld:lifeskim |
pubmed-article:12757612 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:12757612 | pubmed:dateCreated | 2003-5-21 | lld:pubmed |
pubmed-article:12757612 | pubmed:abstractText | This review attempts to illuminate the glycolipid antigen presentation properties of CD1d, how CD1d controls the function of natural T (iNKT) cells and how CD1d and iNKT cells interact to jump-start the immune system. It is postulated that the CD1d-iNKT cell system functions as a sensor, sensing alterations in cellular lipid content by virtue of its affinity for such ligands. The presentation of a neo-self glycolipid, presumably by infectious assault of antigen-presenting cells, activates iNKT cells, which promptly release pro-inflammatory and anti-inflammatory cytokines and jump-start the immune system. | lld:pubmed |
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