Augmentation of natural killer cell activity by lipopolysaccharide through separable effects on the binding of nonadherent lymphocytes to tumor targets and tumor killing

R. A. Salata, M. E. Kleinhenz, B. Z. Schacter, J. J. Ellner

Research output: Contribution to journalArticle

Abstract

A single-cell assay was utilized to study the augmentation by Escherichia coli lipopolysaccharide (LPS) of the cytotoxicity of human lymphocytes for the human myeloid tumor K562. Preincubation with LPS at 20 μg/ml for 30 min at 37° increased the binding of all nonadherent (NA) lymphocytes populations to K562 tumors [unseparated NA lymphocytes from 13.1 to 25.1%, immunoglobulin G Fc receptor-enriched lymphocytes from 27.6 to 42.9%, and immunoglobulin G Fc receptor-depleted lymphocytes from 14.0 to 23.7%, at p <0.001]. In contrast, interferon (IFN) at 10 units/ml had no effect on the overall binding of lymphocytes to K562 tumors. When lymphocyte-tumor conjugates were dispersed in agarose, cytotoxic activity of unseparated NA lymphocytes at 1 to 3 hr was markedly increased by preincubation with LPS (p <0.001). However, LPS did not enhance cytotoxicity if conjugates were formed in its absence. IFN, likewise, increased cytotoxic activity in unseparated NA lymphocytes at 1 to 3 hr (p <0.001). No synergistic cytotoxicity was seen with concurrent exposure to LPS and IFN. LPS increased cytotoxicity in the Fc receptor-enriched tumor conjugates at 1 to 3 hr (p <0.001) and appeared to promote more efficient killing in individual conjugates was not enhanced by LPS. Thus, LPS may enhance natural killer cell-like activity by increasing the binding of human lymphocytes to K562 tumors and by rearranging the population of binding cells to include more efficient killer cells. While the effects of LPS on binding appear independent of IFN, selective recruitment of more efficient killer cells could be through an IFN mechanism.

Original languageEnglish (US)
Pages (from-to)1044-1047
Number of pages4
JournalCancer Research
Volume44
Issue number3
StatePublished - 1984
Externally publishedYes

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

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