| pubmed-article:17609265 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0020094 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0086427 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0332307 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0567416 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0022688 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0063695 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0301896 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0024518 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C1510802 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C1332714 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0439859 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0392756 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C2709199 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0301630 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0456387 | lld:lifeskim |
| pubmed-article:17609265 | lifeskim:mentions | umls-concept:C0205225 | lld:lifeskim |
| pubmed-article:17609265 | pubmed:issue | 18 | lld:pubmed |
| pubmed-article:17609265 | pubmed:dateCreated | 2007-8-30 | lld:pubmed |
| pubmed-article:17609265 | pubmed:abstractText | Although natural killer (NK) cell-mediated control of viral infections is well documented, very little is known about the ability of NK cells to restrain human T-cell leukemia virus type 1 (HTLV-1) infection. In the current study we show that NK cells are unable to kill HTLV-1-infected primary CD4+ T cells. Exposure of NK cells to interleukin-2 (IL-2) resulted in only a marginal increase in their ability to kill HTLV-1-infected primary CD4+ T cells. This inability of NK cells to kill HTLV-1-infected CD4+ T cells occurred despite the down-modulation of major histocompatibility complex (MHC) class I molecules, one of the ligands for the major NK cell inhibitory receptor, by HTLV-1 p12(I) on CD4+ T cells. One reason for this diminished ability of NK cells to kill HTLV-1-infected cells was the decreased ability of NK cells to adhere to HTLV-1-infected cells because of HTLV-1 p12(I)-mediated down-modulation of intercellular adhesion molecule 1 (ICAM-1) and ICAM-2. We also found that HTLV-1-infected CD4+ T cells did not express ligands for NK cell activating receptors, NCR and NKG2D, although they did express ligands for NK cell coactivating receptors, NTB-A and 2B4. Thus, despite HTLV-1-mediated down-modulation of MHC-I molecules, HTLV-1-infected primary CD4+ T cells avoids NK cell destruction by modulating ICAM expression and shunning the expression of ligands for activating receptors. | lld:pubmed |
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| pubmed-article:17609265 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17609265 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17609265 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:17609265 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
