Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1988-8-31
pubmed:abstractText
This study showed that a mAb (145-2C11) against the T3 epsilon-chain of the TCR complex augmented the cytotoxic activity of the lymphokine-activated killer (LAK) effectors. The LAK cells were induced by culturing normal spleen cells with purified human rIL-2. Adding alpha T3 at the effector phase of the cytotoxic reactions augmented the LAK-mediated cytotoxicity. The alpha T3-augmented LAK killing was seen only with tumor targets, and there was no increase of killing against Con A-induced lymphoblasts. The augmentation effect was dose dependent on both the amounts of alpha T3 and the number of LAK cells added. A very low concentration of alpha T3 (1/10,000 dilution of culture supernatants) was sufficient to induce alpha T3-augmented LAK-mediated cytotoxicity. Human rIL-2 at 10 to 30 U/ml was sufficient to generate LAK cells for maximal alpha T3 augmentation, whereas 300 to 1000 U/ml of IL-2 were needed to generate maximal LAK activity when tested in the absence of alpha T3. LAK cells generated for longer periods of time showed a progressive increase of alpha T3-augmented cytotoxicity. For some targets, the alpha T3-augmented LAK killing was FcR dependent as evidenced by the ability of alpha FcR mAb 2.4G2 to inhibit, and for others it was not inhibited. The alpha T3-augmented killing did not correlate with the FcR expression on target cells as defined by 2.4G2. The LAK cells were both Lyt-2+ and Lyt-2-, but the LAK cells involved in alpha T3-augmented killing were exclusively Lyt-2+. Preincubation of LAK cells with alpha T3, but not preincubation of targets with alpha T3, resulted in augmented killing suggesting that the alpha T3 effect was unrelated to an antibody-dependent cell-mediated cytotoxicity. Our findings indicate that alpha T3 is a potent reagent to augment the cytotoxic reaction of LAK cells. These results suggested that a relationship might exist between the T3 complex and the cytotoxic activity of a subpopulation of Lyt-2+ LAK cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
141
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
741-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:3260909-Adjuvants, Immunologic, pubmed-meshheading:3260909-Animals, pubmed-meshheading:3260909-Antibodies, Monoclonal, pubmed-meshheading:3260909-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:3260909-Binding, Competitive, pubmed-meshheading:3260909-Binding Sites, Antibody, pubmed-meshheading:3260909-Cell Line, pubmed-meshheading:3260909-Cytotoxicity, Immunologic, pubmed-meshheading:3260909-Dose-Response Relationship, Immunologic, pubmed-meshheading:3260909-Female, pubmed-meshheading:3260909-Killer Cells, Natural, pubmed-meshheading:3260909-Lymphocyte Activation, pubmed-meshheading:3260909-Lymphokines, pubmed-meshheading:3260909-Mice, pubmed-meshheading:3260909-Mice, Inbred C57BL, pubmed-meshheading:3260909-Mice, Inbred DBA, pubmed-meshheading:3260909-Phenotype, pubmed-meshheading:3260909-Receptors, Fc, pubmed-meshheading:3260909-Spleen, pubmed-meshheading:3260909-Time Factors
pubmed:year
1988
pubmed:articleTitle
Augmentation by anti-T3 antibody of the lymphokine-activated killer cell-mediated cytotoxicity.
pubmed:affiliation
Experimental Immunology Branch, National Cancer Institute, Bethesda, MD 20892.
pubmed:publicationType
Journal Article