Cytokine effects and role of adhesive proteins and Fc receptors in human macrophage‐mediated antibody dependent cellular cytotoxicity

Jane L. Liesveld, Karen E. Frediani, Jill M. Winslow, Camille N. Abboud, Reggie E. Duerst

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

Mononuclear phagocytes participate in host immunological defense against tumors. We have investigated the role of selected recombinant cytokines on human macrophage‐mediated tumor cytotoxicity in vitro utilizing a human colon cancer cell line target, SW1116, and murine monoclonal antibody 17‐1A. Blood monocytes were kept in continuous culture to allow differentiation into macrophages. Maximum antibody dependent cellular cytotoxicity (ADCC) as measured in a 3H‐thymidine release assay occurred after culturing the monocytes for 5–7 days. Human recombinant macrophage colony stimulating factor (CSF) (1,000 U/ml) did not increase ADCC above control levels whereas recombinant human granulocyte‐macrophage colony stimulating factor, interleukin 4, and interleukin 3 were all capable of increasing ADCC. Antibodies to the CD11/CD18 integrin receptors did not significantly inhibit ADCC. When the ADCC incubation occurred in the presence of antibodies to the human Fc receptors, ADCC was inhibited significantly only by anti‐FcRIII (3G8). A role for tumor necrosis factor alpha or other soluble mediators of cytotoxicity was not demonstrable in this system. These studies suggest avenues for manipulation and augmentation of macrophagemediated antitumor ADCC.

Original languageEnglish
Pages (from-to)381-390
Number of pages10
JournalJournal of cellular biochemistry
Volume45
Issue number4
DOIs
StatePublished - Apr 1991

Keywords

  • ADCC
  • cytokine
  • human colon cancer
  • macrophages
  • tumors

Fingerprint Dive into the research topics of 'Cytokine effects and role of adhesive proteins and Fc receptors in human macrophage‐mediated antibody dependent cellular cytotoxicity'. Together they form a unique fingerprint.

Cite this