Expression and function of the early activation antigen CD69 in murine macrophages

CD69, a member of the natural killer cell gene complex family of signal transducing receptors, represents one of the earliest activation antigens in human and murine lymphocytes. In contrast, human monocytes may express CD69 in a constitutive fashion. We have evaluated the expression and function of...

Full description

Saved in:
Bibliographic Details
Published inJournal of leukocyte biology Vol. 62; no. 3; pp. 349 - 355
Main Authors Marzio, Rosa, Jirillo, Emilio, Ransijn, Adriana, Mauël, Jacques, Corradin, Sally Betz
Format Journal Article
LanguageEnglish
Published United States Society for Leukocyte Biology 01.09.1997
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:CD69, a member of the natural killer cell gene complex family of signal transducing receptors, represents one of the earliest activation antigens in human and murine lymphocytes. In contrast, human monocytes may express CD69 in a constitutive fashion. We have evaluated the expression and function of CD69 in murine bone marrow‐derived macrophages. CD69 expression as determined by flow cytometry was not constitutive but was induced by stimulation with interferon‐γ (IFN‐γ) plus bacterial lipopolysaccharide (LPS) or tumor necrosis factor α (TNF‐α). Stimulation with LPS alone was equally effective. Infection with the protozoan parasite Leishmania did not induce CD69 expression nor influence CD69 up‐regulation by IFN‐γ plus LPS. Induction of CD69 expression was significantly inhibited in the presence of prostaglandin E2 or dibutyryl‐cAMP. Stimulation of macrophages with anti‐CD69 monoclonal antibody in the presence of IFN‐γ induced both nitric oxide production and TNF‐α release. Moreover, anti‐CD69 stimulation of Leishmania‐infected macrophages resulted in elimination of the intracellular parasite. These results suggest that CD69 is an activation antigen for murine macrophages and may serve as a signaling receptor for an as yet uncharacterized ligand. J. Leukoc. Biol. 62: 349–355; 1997.
Bibliography:ObjectType-Article-2
SourceType-Scholarly Journals-1
ObjectType-Feature-1
content type line 23
ObjectType-Article-1
ObjectType-Feature-2
ISSN:0741-5400
1938-3673
DOI:10.1002/jlb.62.3.349