Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1980 Jul;125(1):6-12.

Characterization of a human macrophage-like cell line stimulated in vitro: a model of macrophage functions

  • PMID: 7381211

Characterization of a human macrophage-like cell line stimulated in vitro: a model of macrophage functions

J W Larrick et al. J Immunol. 1980 Jul.

Abstract

When cells of human macrophage-like cell line U937 are cultured in the presence of medium conditioned by mixed lymphocyte culture (MLC), PHA- or Con A-stimulated lymphocytes they demonstrate morphologic and functional characteristics of stimulation. The cells become larger, their surface more villous, and the cytoplasm has increased numbers of lysosomes and phagosomes. There is a marked (at least 10-fold) increase in antibody-dependent cellular cytotoxicity (ADCC) against both erythroid and tumor targets accompanied by increased expression of Fc receptors (FcR). There is also an augmentation of antibody-dependent phagocytosis. Medium conditioned by unstimulated lymphocytes, a B lymphoblastoid cell line or a fibroblast cell line produce very little stimulation of U937 cells. U937 cells gradually lose their increased ADCC capacity if they are washed free of conditioned medium (CM) but can be maintained in a stimulated state for long periods of time by culturing them in medium supplemented with PHA-CM at a concentration of 2%. Stimulation of macrophage-like cell line U937 may provide a useful model for further study of mechanisms of macrophage cytotoxicity and its modulation by products of activated lymphocytes.

PubMed Disclaimer

Similar articles

Cited by

Publication types

LinkOut - more resources