| pubmed-article:2459230 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:2459230 | lifeskim:mentions | umls-concept:C0027651 | lld:lifeskim |
| pubmed-article:2459230 | lifeskim:mentions | umls-concept:C0021756 | lld:lifeskim |
| pubmed-article:2459230 | lifeskim:mentions | umls-concept:C0021758 | lld:lifeskim |
| pubmed-article:2459230 | lifeskim:mentions | umls-concept:C0301872 | lld:lifeskim |
| pubmed-article:2459230 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
| pubmed-article:2459230 | lifeskim:mentions | umls-concept:C2348628 | lld:lifeskim |
| pubmed-article:2459230 | pubmed:issue | 8 | lld:pubmed |
| pubmed-article:2459230 | pubmed:dateCreated | 1988-11-9 | lld:pubmed |
| pubmed-article:2459230 | pubmed:abstractText | The relative contributions of IL-2 and IL-4 during the immune response to the retrovirus-induced tumor, FBL, were examined. Both proliferative and cytolytic responses to FBL were measured and compared to similar responses to minor histocompatibility Ag. The addition of alpha IL-2 partially inhibited FBL-stimulated proliferation of purified L3T4+ T cells and nearly completely inhibited the response of Lyt-2+ T cells, whereas alpha IL-4 partially inhibited the proliferative response of the L3T4+ subset but had no effect on the response of the Lyt-2+ subset. The addition of exogenous IL-4 augmented the proliferative response of both subsets. Therefore, IL-4 is an endogenous growth factor for FBL-induced specific proliferation of the L3T4+ and not the Lyt-2+ population, but both subpopulations can respond to IL-4. Similar examination of anti-FBL CTL responses revealed that alpha IL-2, but not alpha IL-4, inhibited FBL-specific Lyt-2+ CTL generation. However, exogenous IL-4 partially replaced the L3T4+ Th cell activity necessary for optimal Lyt-2+ FBL-specific CTL generation. Therefore, IL-4 is not required but can participate in the CTL response. The role of IL-4 during the immune response of B6 mice to minor histocompatibility Ag disparate BALB.B cells was analyzed. alpha IL-4 had no detectable effect on the proliferative or cytolytic response to BALB.B cells, suggesting that endogenous IL-4 does not have a significant role in these responses. The extent of involvement of endogenous IL-4 in the T cell responses to retrovirus-induced tumor Ag and minor histocompatibility Ag presumably reflects the nature of the stimulating Ag, and detection of an IL-4 response may correlate with induction of an antibody response. Thus, the immunizing Ag and/or host B cell repetoire may influence which subsets of L3T4+ Th cells are activated during priming in vivo. | lld:pubmed |
| pubmed-article:2459230 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:2459230 | pubmed:language | eng | lld:pubmed |
| pubmed-article:2459230 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2459230 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:2459230 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2459230 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2459230 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2459230 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2459230 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:2459230 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:2459230 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:2459230 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:2459230 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:2459230 | pubmed:author | pubmed-author:CheeverM AMA | lld:pubmed |
| pubmed-article:2459230 | pubmed:author | pubmed-author:GreenbergP... | lld:pubmed |
| pubmed-article:2459230 | pubmed:author | pubmed-author:KerrD ADA | lld:pubmed |
| pubmed-article:2459230 | pubmed:author | pubmed-author:PeachD MDM | lld:pubmed |
| pubmed-article:2459230 | pubmed:author | pubmed-author:KlarnetJ PJP | lld:pubmed |
| pubmed-article:2459230 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:2459230 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:2459230 | pubmed:volume | 141 | lld:pubmed |
| pubmed-article:2459230 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:2459230 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:2459230 | pubmed:pagination | 2824-30 | lld:pubmed |
| pubmed-article:2459230 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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| pubmed-article:2459230 | pubmed:meshHeading | pubmed-meshheading:2459230-... | lld:pubmed |
| pubmed-article:2459230 | pubmed:year | 1988 | lld:pubmed |
| pubmed-article:2459230 | pubmed:articleTitle | Il-4 is an endogenous T cell growth factor during the immune response to a syngeneic retrovirus-induced tumor. | lld:pubmed |
| pubmed-article:2459230 | pubmed:affiliation | Department of Microbiology/Immunology, University of Washington, Seattle 98195. | lld:pubmed |
| pubmed-article:2459230 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:2459230 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |
| pubmed-article:2459230 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:2459230 | lld:pubmed |
