| pubmed-article:1531321 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:1531321 | lifeskim:mentions | umls-concept:C0007634 | lld:lifeskim |
| pubmed-article:1531321 | lifeskim:mentions | umls-concept:C0024204 | lld:lifeskim |
| pubmed-article:1531321 | lifeskim:mentions | umls-concept:C0312740 | lld:lifeskim |
| pubmed-article:1531321 | lifeskim:mentions | umls-concept:C0178539 | lld:lifeskim |
| pubmed-article:1531321 | lifeskim:mentions | umls-concept:C0021764 | lld:lifeskim |
| pubmed-article:1531321 | lifeskim:mentions | umls-concept:C1704675 | lld:lifeskim |
| pubmed-article:1531321 | lifeskim:mentions | umls-concept:C1718423 | lld:lifeskim |
| pubmed-article:1531321 | lifeskim:mentions | umls-concept:C0079411 | lld:lifeskim |
| pubmed-article:1531321 | lifeskim:mentions | umls-concept:C0127400 | lld:lifeskim |
| pubmed-article:1531321 | pubmed:issue | 5 | lld:pubmed |
| pubmed-article:1531321 | pubmed:dateCreated | 1992-3-18 | lld:pubmed |
| pubmed-article:1531321 | pubmed:abstractText | Previous studies have demonstrated that progressive growth of the weakly immunogenic MCA 106 murine sarcoma stimulated, in the draining lymph nodes, the production of tumor-sensitized but not fully functional preeffector lymphocytes. These lymphocytes could develop into specific immune effector cells after sequential in vitro activation with anti-CD3 monoclonal antibody and interleukin 2 (IL-2). In this study, we analyzed cellular requirements for in vivo sensitization of preeffector cells, for generation of immune effector cells by the method of anti-CD3/IL-2 activation, and for adoptive immunotherapy mediated by activated cells. By selective depletion of T-cell subsets in vivo, we found that tumor regression after systemic adoptive immunotherapy required the collaboration of activated CD4+ and CD8+ cells. It was further demonstrated that CD8+ immune cells alone could mediate antitumor effects if exogenous IL-2 was provided in vivo. These results suggest that CD8+ cells served as immediate effector cells, whereas CD4+ immune cells provided a helper function via the secretion of IL-2. During in vitro anti-CD3/IL-2 activation, generation of effector cells depended on the collaborative interaction between previously sensitized CD4+ and CD8+ preeffector cells. At the stage of in vitro activation, the addition of IL-2 could not substitute the function of CD4+ cells. We next examined whether the sensitization of preeffector cells in the draining lymph nodes required cellular interactions between CD4+ and CD8+ T-cells. By in vivo depletion of T-cell subsets during tumor growth, we found that CD4+ cells were sensitized independently of CD8+ cells. More interestingly, in vivo sensitization of CD8+ preeffector cells also occurred independently in the absence of a CD4+ helper cell response. The lack of T-cell-T-cell interactions in vivo may explain the failure of effector cell generation during progressive tumor growth. Taken together, these results demonstrate that the anti-CD3/IL-2 activation defines an immune response distinct from many previously described mechanisms of antitumor immune responses. | lld:pubmed |
| pubmed-article:1531321 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1531321 | pubmed:language | eng | lld:pubmed |
| pubmed-article:1531321 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1531321 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:1531321 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1531321 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1531321 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1531321 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1531321 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1531321 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:1531321 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:1531321 | pubmed:month | Mar | lld:pubmed |
| pubmed-article:1531321 | pubmed:issn | 0008-5472 | lld:pubmed |
| pubmed-article:1531321 | pubmed:author | pubmed-author:ChangA EAE | lld:pubmed |
| pubmed-article:1531321 | pubmed:author | pubmed-author:YoshizawaHH | lld:pubmed |
| pubmed-article:1531321 | pubmed:author | pubmed-author:MaaY HYH | lld:pubmed |
| pubmed-article:1531321 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:1531321 | pubmed:day | 1 | lld:pubmed |
| pubmed-article:1531321 | pubmed:volume | 52 | lld:pubmed |
| pubmed-article:1531321 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:1531321 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:1531321 | pubmed:pagination | 1129-36 | lld:pubmed |
| pubmed-article:1531321 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
| pubmed-article:1531321 | pubmed:meshHeading | pubmed-meshheading:1531321-... | lld:pubmed |
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| pubmed-article:1531321 | pubmed:meshHeading | pubmed-meshheading:1531321-... | lld:pubmed |
| pubmed-article:1531321 | pubmed:meshHeading | pubmed-meshheading:1531321-... | lld:pubmed |
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| pubmed-article:1531321 | pubmed:meshHeading | pubmed-meshheading:1531321-... | lld:pubmed |
| pubmed-article:1531321 | pubmed:year | 1992 | lld:pubmed |
| pubmed-article:1531321 | pubmed:articleTitle | Cellular interactions in effector cell generation and tumor regression mediated by anti-CD3/interleukin 2-activated tumor-draining lymph node cells. | lld:pubmed |
| pubmed-article:1531321 | pubmed:affiliation | Department of Surgery, University of Michigan, Ann Arbor 48109. | lld:pubmed |
| pubmed-article:1531321 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:1531321 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:1531321 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1531321 | lld:pubmed |
| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:1531321 | lld:pubmed |
