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CD18/CD54(+CD102), CD2/CD58 Pathway-Independent Killing of Lymphokine-Activated Killer (LAK) Cells Against Glioblastoma Cell Lines T98G and U373MG

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Abstract:

For natural killer cell-mediated cytolysis (NK-lysis) and lymphokine-activated killer cell-mediated cytolysis (LAK-lysis), the co-stimulatory signals of CD18/CD54(+CD102) and CD2/CD58 pathways are essential. However, in this report, we describe a LAK-lysis that does not depend upon these two pathways. The killed cells were glioblastoma cell lines T98G and U373MG. The LAK cells were induced from peripheral blood lymphocytes in the presence of interleukin-2. 1) The T98G and U373MG did not express CD54 or CD102, but expressed CD58. 2) However, when they were pretreated with an anti-CD58 (TS2/9), the LAK-lysis was not blocked. 3) The LAK-lysis was markedly inhibited by pretreating with Concanamycin A and slightly inhibited by treating with antitumor necrosis factor-related apoptosis-inducing ligand (anti-TRAIL) antibody. 4) Nineteen percent of the LAK cells adhered to the T98G. The adhered LAK cells killed it. But nonadherent LAK cells could not kill the T98G or U373MG but killed lymphoblastoma cell lines Raji and NALM-6. These findings suggested that this type of the LAK-lysis might not depend upon the CD18/CD54(+CD102) pathway or CD2/CD58 pathway. The effector cells that killed the T98G and U373MG might not always be the same as the effector cells that killed the other cell lines. The LAK cells contain several subsets, and one of the subsets might kill these two target cell lines.

Keywords: Adhes; Key words: Lymphokine-activated killer cell

Document Type: Research Article

DOI: http://dx.doi.org/10.3727/000000001108747408

Affiliations: Blood Transfusion Service, School of Medicine, Tokyo Medical and Dental University, Yushima 1-5-45, Bunkyoku, Tokyo 113-8519, Japan

Publication date: January 1, 2001

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  • Formerly: Oncology Research Incorporating Anti-Cancer Drug Design
    Oncology Research Featuring Preclinical and Clincal Cancer Therapeutics publishes research of the highest quality that contributes to an understanding of cancer in areas of molecular biology, cell biology, biochemistry, biophysics, genetics, biology, endocrinology, and immunology, as well as studies on the mechanism of action of carcinogens and therapeutic agents, reports dealing with cancer prevention and epidemiology, and clinical trials delineating effective new therapeutic regimens.
cog/or/2001/00000012/00000001/or211
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