Induction of murine macrophage TNF-α synthesis byMycobacterium aviumis modulated through complement-dependent interaction via complement receptors 3 and 4 in relation toM. aviumglycopeptidolipid
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چکیده
منابع مشابه
Macrophage Complement
Circulating monocytes and tissue macrophages (Me) 1 secrete complement proteins and have distinct receptors for some of these secreted products. Although hepatocytes and possibly epithelial cells are major sources of plasma complement (1), Mcl synthesize C1 subcomponents (2, 3), C4 (4, 5), C2 (5-7) C5 (8), C3 (2, 8) and all the components of the alternative pathway and its control proteins (8)....
متن کاملLocal opsonization by secreted macrophage complement components. Role of receptors for complement in uptake of zymosan
We have examined the role of macrophage (M phi plasma membrane receptors for the cleaved third complement component (iC3b; CR3) and mannosyl, fucosyl terminated glycoproteins (MFR) in uptake of unopsonized zymosan. Monoclonal antibodies against CR3, M1/70 (Mac-1) and MO1, each inhibited approximately 50% of uptake of 125I-zymosan by murine and human M phi, respectively. Yeast mannan inhibited 0...
متن کاملInteraction of human monocytes, macrophages, and polymorphonuclear leukocytes with zymosan in vitro. Role of type 3 complement receptors and macrophage-derived complement.
Macrophages take up zymosan in the absence of exogenous complement via receptors for iC3b (type 3 complement receptors) acting with or without lectin-like receptors for mannosyl-fucosyl-terminated glycoconjugates. We previously provided evidence that macrophages themselves secrete complement-alternative pathway components able to opsonize zymosan locally (Ezekowitz et al., J. Exp. Med. 1984. 15...
متن کاملDeficiency of DAF and Crry on murine platelets leads to complement-dependent clearance via the macrophage phagocytic receptor CRIg
Address correspondence and reprint requests to: Dr. Wen-Chao Song Institute for Translational Medicine and Therapeutics and Department of Pharmacology University of Pennsylvania School of Medicine, Rm 1254 BRBII/III, 421 Curie Blvd Philadelphia, PA 19104, Tel: 215-573-6641, Fax: 215-746-8941 [email protected] Blood First Edition Paper, prepublished online June 4, 2008; DOI 10.1182/bloo...
متن کاملGluR3 autoantibodies destroy neural cells in a complement-dependent manner modulated by complement regulatory proteins.
GluR3 autoantibodies have been implicated in the development of Rasmussen's encephalitis, a rare neurodegenerative disease of humans characterized by epilepsy and degeneration of a single cerebral hemisphere. GluR3 autoantibodies are found in some Rasmussen's encephalitis patients, and GluR3 antibodies raised in rabbits destroy cultured cortical cells in a complement-dependent manner. In this s...
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ژورنال
عنوان ژورنال: FEMS Microbiology Letters
سال: 2005
ISSN: 0378-1097,1574-6968
DOI: 10.1016/j.femsle.2005.04.008