Linked Life Data

1975566

Source:http://linkedlifedata.com/resource/pubmed/id/1975566

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1990-10-9
pubmed:abstractText
The primary activation pathway of T cells is via the T-cell receptor (TCR)/CD3 complex, which is functionally interrelated with various accessory molecules. We examined the contribution of the lymphocyte-function-associated antigen-I/intercellular adhesion molecule 1 (LFA-1/ICAM-1) interaction to CD3/TCR-mediated lysis by cytotoxic T lymphocytes (CTL). We used ICAM-I-or+ tumor cell lines as target cells and anti-CD3- or anti-LFA-1 containing hetero-cross-linked monoclonal antibody (MAb) to bridge CTL and target cells and simultaneously to activate CTL. The ICAM-1- melanoma-derived cell line IgR39 was relatively resistant to CD3-mediated lysis by both TCR alpha beta + and TCR gamma delta + CTL, when compared with ICAM-1+ cell lines. Induction of ICAM-1 on the membrane of IgR39 cells by tumor necrosis factor (TNF) rendered these cells more susceptible to CD3-mediated lysis. Anti-ICAM-1 MAb inhibited this TNF-enhanced susceptibility to lysis, directly demonstrating that the induction of ICAM-1 was critical in the TNF-induced increase in susceptibility to lysis of IgR39 cells. CTL formed less efficient conjugates with the ICAM-1- cells as compared to ICAM-1+ cells. Both spontaneous and CD3-induced conjugate formation as well as CD3-mediated lysis of ICAM-1- tumor cells by CTL were enhanced by the addition of anti-LFA-1 containing hetero-cross-linked MAb, thereby mimicking the LFA-1/ICAM-1 interaction between CTL and target cells. Soluble anti-CD18 MAb inhibited CD3-mediated lysis of ICAM-1- target cells by CTL without affecting their conjugate formation. Anti-LFA-1 MAb added after conjugate formation still inhibited lysis of both ICAM-1+or- tumor cells. Taken together, these findings suggest that the LFA-1/ICAM-1 interaction co-activates CD3/TCR-mediated lysis by CTL through both an enhanced CTL-target cell binding and the delivery of post-conjugate costimulatory signals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0020-7136
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
475-80
pubmed:dateRevised
2007-7-24
pubmed:meshHeading
pubmed-meshheading:1975566-Antibodies, Monoclonal, pubmed-meshheading:1975566-Antigens, CD3, pubmed-meshheading:1975566-Antigens, Differentiation, pubmed-meshheading:1975566-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:1975566-Cell Adhesion Molecules, pubmed-meshheading:1975566-Cell Communication, pubmed-meshheading:1975566-Humans, pubmed-meshheading:1975566-Intercellular Adhesion Molecule-1, pubmed-meshheading:1975566-Lymphocyte Activation, pubmed-meshheading:1975566-Lymphocyte Function-Associated Antigen-1, pubmed-meshheading:1975566-Melanoma, pubmed-meshheading:1975566-Receptors, Antigen, T-Cell, pubmed-meshheading:1975566-Receptors, Leukocyte-Adhesion, pubmed-meshheading:1975566-Signal Transduction, pubmed-meshheading:1975566-T-Lymphocytes, Cytotoxic, pubmed-meshheading:1975566-Tumor Cells, Cultured
pubmed:year
1990
pubmed:articleTitle
ICAM- melanoma cells are relatively resistant to CD3-mediated T-cell lysis.
pubmed:affiliation
Dept. of Immunology, Dr. Daniel den Hoed Cancer Center, Rotterdam, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't