Search results for "complement pathway"
showing 10 items of 70 documents
The Clinical Enzymology of the Complement System
1989
The complement (C) system is one of the most important humoral systems mediating many activities that contribute to inflammation and host defense, e.g. various anaphylatoxin activities, Chemotaxis and opsonization for phagocytosis. The C system is similar to other humoral systems, such as coagulation, fibrinolysis and the kinin system, a multifactoral system whose activation represents sequentially occurring multi-step activation cascades of the “classical” as well as the “alternative” pathway.
Components of an antigen-/T cell receptor-independent pathway of lymphokine production
1991
The general way to induce the synthesis of lymphokines by T cells is the stimulation through the T cell receptor (TcR) complex which results in an increase of intracellular [Ca2+] and in the activation of a tyrosine kinase as well as of protein kinase C. Lymphokine production induced via the TcR is inhibited by the immunosuppressive drug cyclosporin A (CsA). However, an alternative pathway of lymphokine production exists. Several T lymphocyte clones can synthesize interferon-gamma (IFN-gamma), granulocyte-monocyte colony-stimulating factor, and small amounts of interleukin (IL3) when stimulated with syngeneic or allogeneic accessory cells (AC) plus IL2. In contrast to the TcR pathway the al…
Alternative pathway activation of T cells by binding of CD2 to its cell-surface ligand.
1987
Activation of resting T lymphocytes is initiated by the interaction of cell-surface receptors with their corresponding ligands. In addition to activation through the CD3 (T3)-Ti antigen-receptor complex1, recent experiments have demonstrated induction of T-cell proliferation through the CD2 (T11) molecule2–4, traditionally known as the erythrocyte(E)-receptor, through which T cells can bind red blood cells (RBC)5–7. This 'alternative pathway' of T-cell activation2 was observed in vitro in response to combinations of anti-CD2 monoclonal antibodies (mAbs) that bind to distinct epitopes of CD2, such as mAbs against T112 plus T113 (ref. 2). The physiological importance of this activation pathwa…
Role of the virulence plasmid pR99 and the metalloprotease Vvp in resistance of Vibrio vulnificus serovar E to eel innate immunity
2007
Vibrio vulnificus biotype 2 serovar E (VSE) is a bacterial pathogen that produces a haemorrhagic septicaemia called vibriosis in eels. Its ability to grow in blood is conferred by a recently described virulence plasmid [Lee CT, Amaro C, Wu KM, Valiente E, Chang YF, Tsai SF, et al. A common virulence plasmid in biotype 2 Vibrio vulnificus and its dissemination aided by a conjugal plasmid. Journal of Bacteriology, submitted for publication.]. In this study, we analyzed the role of this plasmid together with the role played by the metalloprotease (Vvp) in the interaction between bacteria and eel innate immunity. To this end, we compared and statistically analyzed the differences in resistance …
Isolation and characterization of a complement-activating lipid extracted from human atherosclerotic lesions.
1990
The major characteristics of human atherosclerotic lesions are similar to those of a chronic inflammatory reaction, namely fibrosis, mesenchymal cell proliferation, the presence of resident macrophages, and cell necrosis. Atherosclerosis exhibits in addition the feature of lipid (mainly cholesterol) accumulation. The results of the present report demonstrate that a specific cholesterol-containing lipid particle present in human atherosclerotic lesions activates the complement system to completion. Thus, lipid could represent a stimulatory factor for the inflammatory reaction, whose underlying mechanistic basis may be, at least in part, complement activation. The complement-activating lipid …
An inherited deficiency of the third component of complement, C3, in guinea pigs
1986
Hereditary deficiency of the third component of complement, C3, is found very seldom in the human. C3 deficiency is associated with severe bacterial infections revealing the central role of C3 in complement activation via the classical or alternative pathway. We describe a new hereditary C3 deficiency in strain 2 guinea pigs. Serum from these animals had a markedly reduced lytic activity in a standard assay for complement-dependent, antibody-mediated cytotoxicity. In functional assays of individual components, the hemolytic activity of the components C4, C2, C5 and of factors B, D and H was in the normal range. The functional C3 titer, and similarly C3 antigenic activity in the serum of the…
C1-esterase inhibitor in ischemia and reperfusion.
2002
Summary Myocardial injury from ischemia can be aggravated by reperfusion of the jeopardized area. The precise underlying mechanisms have not been clearly defined, but proinflammatory events including complement activation play important roles. Cardioprotection by complement inhibition inter alia C1-esterase-inhibitor (C1-INH) was examined in several experimental models and under clinical conditions with ischemia and reperfusion. C1-INH reduced local anaphylatoxin release revealing the importance of the classical complement pathway. Inhibition of local complement activation was accompanied by improvement of myocardial function and perfusion of the previously ischemic myocardium. Leukocyte en…
Studies on the mechanism of PMN activation. I. By dextran sulfates.
1982
Evidence is presented that enhanced reduction of the dye nitroblue-tetrazolium (NBT) by polymorphonuclear leukocytes (PMN) which are stimulated by dextran sulfates (DS) is not exclusively due to the phagocytosis of particles formed by NBT and DS. Not only the size of phagocytizable particles but the degree of substitution determines the acceleration of NBT-reduction. A likely cause of this acceleration is the triggering of the alternative pathway of the complement activation.
The Role of the Classical Pathway for the Bactericidal Effect of Normal Sera Against Gram-Negative Bacteria
1985
Many gram-negative bacteria are killed after treatment with normal serum. This phenomenon was already described in 1889 by Buchner. The serum-bactericidal effect is abolished when serum has been incubated for 30 min at 56° C. Gram-positive bacteria are less sensitive than gram-negative bacteria to direct killing, although gram-positive cocci are opsonized by the action of serum mediated by antibodies and complement (Inoue et al. 1968; Johnston et al. 1969). Normal sera exhibit bactericidal and bacteriolytic properties against some gramnegative strains; whereas, other gram-negative strains are serum resistant. It has been shown that serum from C4-deficient guinea pigs is able to kill some gr…
Interaction of Bacterial Endotoxin (LPS) with Fluid Phase and Macrophage Membrane Associated C1q, the FC-Recognizing Component of the Complement Syst…
1990
The bactericidal activity of normal serum was first described by Buchner in 1889 (10). This effect is abolished when serum has been incubated for 30 min at 56°C. Gram positives are less sensitive than Gram negative bacteria to direct killing, although gram positive cocci are opsonized by the action of serum mediated by antibodies and complement (22). It was found that most of the smooth strains of gram negative bacteria are serum resistant; whereas, the corresponding rough forms are extremely serum sensitive (32, 37). Thus evidence was provided that the composition of the bacterial surface may influence the reaction of the bacteria with the lytic system. The bacteriolytic properties of seru…