Human natural cytotoxic activity mediated by tumor necrosis factor: Regulation by interleukin-2

Edmund Lattime, Antonella Stoppacciaro, Amanullah Khan, Osias Stutman

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Freshly obtained normal lymphoid cells kill certain tumor target cells in vitro. Using peripheral-blood lymphocytes (PBLs) and the human tumor target cell line BT-20, we have defined a tumor necrosis factor (TNF)-dependent, cell-mediated cytotoxic mechanism that is homologous to the murine natural cytotoxic (NC) cell activity. Human NC cell activity was detected in freshly isolated PBLs and was augmented by short in vitro pulses with recombinant human interleudin-2 but not with recombinant human alfa interferon. Monoclonal anti-TNF antibodies inhibited the killing of the target cells. The independence of interferon and the mediation of killing by TNF distinguish human NC cell activity from natural killer and lymphokine-activated killer cell activitoes. [J Natl Cancer Inst 1988;80:1035-1038].

Original languageEnglish (US)
Pages (from-to)1035-1038
Number of pages4
JournalJournal of the National Cancer Institute
Volume80
Issue number13
DOIs
StatePublished - Sep 7 1988

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Interleukin-2
Tumor Necrosis Factor-alpha
Lymphocytes
Lymphokine-Activated Killer Cells
Tumor Cell Line
Interferon-alpha
Natural Killer Cells
Interferons
Neoplasms
Antibodies
In Vitro Techniques

All Science Journal Classification (ASJC) codes

  • Oncology
  • Cancer Research

Cite this

Lattime, Edmund ; Stoppacciaro, Antonella ; Khan, Amanullah ; Stutman, Osias. / Human natural cytotoxic activity mediated by tumor necrosis factor : Regulation by interleukin-2. In: Journal of the National Cancer Institute. 1988 ; Vol. 80, No. 13. pp. 1035-1038.
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Human natural cytotoxic activity mediated by tumor necrosis factor : Regulation by interleukin-2. / Lattime, Edmund; Stoppacciaro, Antonella; Khan, Amanullah; Stutman, Osias.

In: Journal of the National Cancer Institute, Vol. 80, No. 13, 07.09.1988, p. 1035-1038.

Research output: Contribution to journalArticle

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