pubmed-article:1987288 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:1987288 | lifeskim:mentions | umls-concept:C0022567 | lld:lifeskim |
pubmed-article:1987288 | lifeskim:mentions | umls-concept:C1518997 | lld:lifeskim |
pubmed-article:1987288 | lifeskim:mentions | umls-concept:C0024348 | lld:lifeskim |
pubmed-article:1987288 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:1987288 | pubmed:dateCreated | 1991-2-20 | lld:pubmed |
pubmed-article:1987288 | pubmed:abstractText | Interleukin 2 (IL-2)-activated peripheral blood mononuclear cells (PBMC) have been reported to lyse tumor cells while essentially sparing normal cells in vitro. This report concerns IL-2-induced anti-keratinocyte (anti-KC) cytotoxic effectors that lyse normal human keratinocytes (KC) in vitro. Effectors were generated by culturing PBMC for 1-8 d in various concentrations of recombinant IL-2 and then assayed against 51Cr-labeled targets. Effectors stimulated with 10(3) U/ml of IL-2 for 8 d readily lysed adherent or trypsinized autologous or allogeneic KC cultured in serum-free medium. Induction of anti-KC effectors was IL-2 dose-dependent, with as little as 12-25 U/ml of IL-2 inducing increased anti-KC activity after 24 h of treatment. Although anti-KC activity was increased after overnight culture in IL-2, maximal effector potency in terms of lytic units (LU) per 10(6) effector cells required 4 d of IL-2 treatment. Maximal effector yield in terms of LU per input PBMC occurred after 8 d of IL-2 treatment. Antibody plus complement depletion studies showed that the anti-KC effectors predominantly have a CD16 --/CD3 --/CD2+ phenotype. A natural killer (NK)-like specificity of the effectors was suggested by two findings: unlabeled K562 cells totally inhibited lysis of 51Cr-KC in cold target competition assays, and interferon gamma (IFN-g) treatment (2.5 U/ml-500 U/ml of recombinant IFN-g for 48-72 h) down-regulated KC susceptibility to lysis by these effectors. Thus, IL-2 treatment of PBMC induces non-T cell, natural killer-like effectors that can lyse both autologous and allogeneic KC. Furthermore, KC resemble other cell types that become resistant to non-MHC-restricted lysis after treatment with IFN-g. Finally, the contrasting effects of IFN-g treatment on KC lysis by these effectors, as opposed to lysis by specific T cells, suggests that IFN-g could promote a shift from non-MHC-restricted to MHC-restricted KC lysis during epidermal immune responses in vivo. | lld:pubmed |
pubmed-article:1987288 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1987288 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1987288 | pubmed:language | eng | lld:pubmed |
pubmed-article:1987288 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1987288 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:1987288 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1987288 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1987288 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:1987288 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:1987288 | pubmed:month | Jan | lld:pubmed |
pubmed-article:1987288 | pubmed:issn | 0022-202X | lld:pubmed |
pubmed-article:1987288 | pubmed:author | pubmed-author:SymingtonF... | lld:pubmed |
pubmed-article:1987288 | pubmed:author | pubmed-author:SantosE BEB | lld:pubmed |
pubmed-article:1987288 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:1987288 | pubmed:volume | 96 | lld:pubmed |
pubmed-article:1987288 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:1987288 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:1987288 | pubmed:pagination | 127-33 | lld:pubmed |
pubmed-article:1987288 | pubmed:dateRevised | 2007-11-14 | lld:pubmed |
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pubmed-article:1987288 | pubmed:year | 1991 | lld:pubmed |
pubmed-article:1987288 | pubmed:articleTitle | Lysis of keratinocytes by IL-2-activated peripheral blood lymphocytes. | lld:pubmed |
pubmed-article:1987288 | pubmed:affiliation | Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington 98104. | lld:pubmed |
pubmed-article:1987288 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:1987288 | pubmed:publicationType | Research Support, U.S. Gov't, P.H.S. | lld:pubmed |