PubMed HealthSearch

PubMed · 1526593

[Complement system: its involvement in the local inflammatory response].

Abstract

The source did not provide an abstract. Follow the original record for more information.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Y Laufer, J Passwell. 1992-05-01. [Complement system: its involvement in the local inflammatory response].. https://pubmed.ncbi.nlm.nih.gov/1526593/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Enhanced IgG- and complement-independent phagocytosis of sulfatide-enriched human erythrocytes by human monocytes.

Phagocytosis by adherent human monocytes of human erythrocytes (RBC), sulfatide-enriched by incubation with 10(-12) to 10(-9) M cerebroside sulfate, was enhanced approx. 6-fold. Increased phagocytosis was observed only in RBC opsonized with fresh plasma, and not in non-opsonized or serum-opsonized RBC. Increased phagocytosis was immunoglobulin- and complement independent. Thrombospondin and von Willebrand factor, present in plasma but not in serum, and binding selectively to sulfatides, are likely mediators of the enhanced phagocytosis.

Complement System Proteins

Localization and characterization of human salivary kininases.

The human saliva of normal subjects containing large amounts of basic carboxypeptidase produces decarboxylated non inflammatory peptides, for instance, kinins and anaphilotoxins C3a, C4a and C5a. A reduction of epithelial cell-bonded enzyme (carboxypeptidase M-type or kininase I), produces inflammations by the active intact kinins and the initiation of the alternative activating pathway of complement by active anaphilotoxins, which generate complement cleavage products, containing potential destructive mechanism.

Complement System Proteins