These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Regulation of a murine macrophage haemagglutinin (sheep erythrocyte receptor) by a species-restricted serum factor.
    Author: Crocker PR, Hill M, Gordon S.
    Journal: Immunology; 1988 Dec; 65(4):515-22. PubMed ID: 3220506.
    Abstract:
    The mechanisms which generate heterogeneity amongst resident tissue macrophages (M phi) are poorly understood. In a previous study we described a novel mouse M phi haemagglutinin, which binds unopsonized sheep erythrocytes. This sheep erythrocyte receptor (SER) is expressed at high levels on stromal M phi from bone marrow and lymph nodes, but at low levels on M phi from serous cavities and broncho-alveolar spaces. In this paper we demonstrate that a species-restricted factor in mouse serum is required in vitro for optimal maintenance of SER on resident bone marrow M phi and for its induction on M phi populations which normally lack this receptor. Using thioglycollate-elicited peritoneal M phi, induction of SER by mouse serum was dose-dependent, reached maximal levels by 3-4 days, required the continuous presence of mouse serum, and was fully reversible. Re-expression following trypsinization was inhibited by cycloheximide, showing that protein synthesis by M phi was necessary. Using a quantitative microtitre plate assay to measure levels of the inducing activity (SER-IA) in different samples, it was found to be heat-labile, non-dialysable, precipitable by polyethylene glycol and inactivated at pH 4 but not at pH 9.6. On gel filtration of mouse serum, a single major peak of activity was obtained with an apparent MW of around 70,000. SER-IA appears to be unrelated to a variety of factors and cytokines which affect M phi function, including colony-stimulating factor-1 (CSF-1). The possible role of SER-IA in regulating the differential expression of SER in vivo is discussed.
    [Abstract] [Full Text] [Related] [New Search]