pubmed-article:9310825 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:9310825 | lifeskim:mentions | umls-concept:C1420192 | lld:lifeskim |
pubmed-article:9310825 | lifeskim:mentions | umls-concept:C1326163 | lld:lifeskim |
pubmed-article:9310825 | pubmed:issue | 9 | lld:pubmed |
pubmed-article:9310825 | pubmed:dateCreated | 1997-10-28 | lld:pubmed |
pubmed-article:9310825 | pubmed:abstractText | CD98 is a 125 kDa heterodimer, which is strongly expressed on the surface of activated and proliferating cells. Its expression is strikingly regulated during T cell differentiation and activation, but the role of CD98 during T lymphocyte responses is not yet understood. We report here that proliferation of resting peripheral blood mononuclear cells (PBMC) induced by lectin, superantigen (SAg) or conventional antigens was blocked by anti-CD98 heavy chain (CD98hc) mAb. In contrast, anti-CD98hc did not block responses of T cell clones or lines. Anti-CD98hc inhibited IL-2 receptor expression and progression of T cells from G1 to S phase, but did not reduce expression of the IL-2 gene. Anti-CD98hc mAb did not regulate the initial activation events involving the TCR and co-receptor structures, but instead inhibited T lymphocyte responses even when added 18 h or more after the activation stimulus. Further experiments demonstrated that anti-CD98 was not directly affecting T cells in this system, but was instead acting on accessory cells. This was supported using a novel xenogeneic system that takes advantage of the lack of xenoreactivity of purified human T cells against mouse splenocytes. Despite absence of a direct xenoresponse to murine spleen cells, human T cells were activated by SAg presented by murine splenic antigen-presenting cells (APC). Murine anti-human CD98hc did not block T cell proliferation in this system. Furthermore, responses using monocyte-depleted PBMC as APC were not blocked by anti-CD98hc. Taken together, the present data suggests that triggering of human monocyte CD98 can suppress T cell proliferation by a process that halts progression through the cell cycle of recently activated T lymphocytes. This may represent a novel pathway for monocyte regulation of T cell activation. | lld:pubmed |
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pubmed-article:9310825 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9310825 | pubmed:language | eng | lld:pubmed |
pubmed-article:9310825 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9310825 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:9310825 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:9310825 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9310825 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9310825 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:9310825 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:9310825 | pubmed:month | Sep | lld:pubmed |
pubmed-article:9310825 | pubmed:issn | 0953-8178 | lld:pubmed |
pubmed-article:9310825 | pubmed:author | pubmed-author:HUHH | lld:pubmed |
pubmed-article:9310825 | pubmed:author | pubmed-author:HanashS MSM | lld:pubmed |
pubmed-article:9310825 | pubmed:author | pubmed-author:OTAM IMI | lld:pubmed |
pubmed-article:9310825 | pubmed:author | pubmed-author:KuickR DRD | lld:pubmed |
pubmed-article:9310825 | pubmed:author | pubmed-author:FriedmanA WAW | lld:pubmed |
pubmed-article:9310825 | pubmed:author | pubmed-author:DiazL ALAJr | lld:pubmed |
pubmed-article:9310825 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:9310825 | pubmed:volume | 9 | lld:pubmed |
pubmed-article:9310825 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:9310825 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:9310825 | pubmed:pagination | 1221-31 | lld:pubmed |
pubmed-article:9310825 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:9310825 | pubmed:year | 1997 | lld:pubmed |
pubmed-article:9310825 | pubmed:articleTitle | Monocyte-dependent regulation of T lymphocyte activation through CD98. | lld:pubmed |
pubmed-article:9310825 | pubmed:affiliation | Rackham Arthritis Research Unit, Department of Internal Medicine, Specialized Center of Research in Rheumatoid Arthritis, Ann Arbor, MI, USA. | lld:pubmed |
pubmed-article:9310825 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:9310825 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
pubmed-article:9310825 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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