Linked Life Data

2891766

Source:http://linkedlifedata.com/resource/pubmed/id/2891766

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1988-2-12
pubmed:abstractText
Stimulatory of antigen-specific murine T cell hybridomas with the appropriate antigen has been shown to cause lymphokine secretion and inhibition of spontaneous cell growth. In this study, the effect of cellular activation on the growth of transformed T cells, of known or unknown antigen specificity, was explored with stimulatory monoclonal antibodies (mAb) that recognize nonclonally distributed T cell surface molecules. Anti-CD3 antibodies stimulated interleukin 2 (IL-2) secretion while they inhibited murine and human T cell tumor growth in vitro. Both responses required external cross-linking of the anti-CD3 antibodies. Activation via two molecules that are not physically associated with the T cell antigen receptor, Thy-1 and Ly-6, also inhibited transformed T cell growth while inducing IL-2 secretion. Notably, an anti-Thy-1 mAb that did not cause the transformed T cells to secrete lymphokines failed to affect their growth, and in fact blocked the growth inhibition induced by the stimulatory mAb. Regardless of which stimulating mAb was used, IL-2 production and cell growth were inversely proportional, manifesting similar antibody dose-response curves. Activation of a T cell hybridoma with stimulatory mAb resulted in rapid lysis, as evidenced by the release of 51Cr and lactate dehydrogenase. Cell cycle analysis demonstrated that cellular activation was accompanied by a cell cycle block between the G1 and S phases, and probably a slowing of the transit of cells already in S. These results demonstrate that the growth of a spectrum of neoplastic T cells, murine and human, can be inhibited by what are normally growth-promoting signals for non-transformed T cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
140
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
324-35
pubmed:dateRevised
2003-11-14
pubmed:meshHeading
pubmed-meshheading:2891766-Animals, pubmed-meshheading:2891766-Antibodies, Monoclonal, pubmed-meshheading:2891766-Antigen-Antibody Reactions, pubmed-meshheading:2891766-Antigens, CD3, pubmed-meshheading:2891766-Antigens, Differentiation, pubmed-meshheading:2891766-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:2891766-Antigens, Ly, pubmed-meshheading:2891766-Antigens, Surface, pubmed-meshheading:2891766-Antigens, Thy-1, pubmed-meshheading:2891766-Cell Cycle, pubmed-meshheading:2891766-Cell Survival, pubmed-meshheading:2891766-Cell Transformation, Neoplastic, pubmed-meshheading:2891766-DNA, pubmed-meshheading:2891766-Hybridomas, pubmed-meshheading:2891766-Interleukin-2, pubmed-meshheading:2891766-Lymphocyte Activation, pubmed-meshheading:2891766-Mice, pubmed-meshheading:2891766-Receptors, Fc, pubmed-meshheading:2891766-T-Lymphocytes
pubmed:year
1988
pubmed:articleTitle
Inhibition of transformed T cell growth in vitro by monoclonal antibodies directed against distinct activating molecules.
pubmed:affiliation
Biological Response Modifiers Program, National Cancer Institute, Bethesda, MD 20892.
pubmed:publicationType
Journal Article