Search results for "Complement C3"
showing 9 items of 69 documents
Suppressive effects of C3b on monocyte-dependent T cell proliferation.
1987
The effect of C3b treatment of human monocytes on secondary antigen-dependent T cell response was studied. When antigen-specific T cell blasts were cultivated together with C3b-treated monocytes the proliferative response was inhibited in a dose-dependent fashion. This suppressive effect was specific for C3b because heat-inactivated C3b or buffer alone had no influence on T cell proliferation. In part, this suppressive effect is mediated through a C3b-induced decreased expression of class II antigens on the surface of treated monocytes, but another suppressive mechanism exists because the C3b pretreatment of monocytes also led to an inhibition of the proliferative response in a class II ant…
Activation of complement by the alternative pathway as a factor in the pathogenesis of periodontal disease.
1976
Dental plaque and a bacterium, Actinomyces viscosus, isolated from plaque that can reproduce periodontal disease in germ-free rats, are activators of complement by the alternative pathway. It is suggested that this process is involved in the pathogenesis of chronic inflammatory periodontal disease.
On the pathogenesis of atherosclerosis: enzymatic transformation of human low density lipoprotein to an atherogenic moiety.
1995
Combined treatment with trypsin, cholesterol esterase, and neuraminidase transforms LDL, but not HDL or VLDL, to particles with properties akin to those of lipid extracted from atherosclerotic lesions. Single or double enzyme modifications, or treatment with phospholipase C, or simple vortexing are ineffective. Triple enzyme treatment disrupts the ordered and uniform structure of LDL particles, and gives rise to the formation of inhomogeneous lipid droplets 10-200 nm in diameter with a pronounced net negative charge, but lacking significant amounts of oxidized lipid. Enzymatically modified LDL (E-LDL), but not oxidatively modified LDL (ox-LDL), is endowed with potent complement-activating c…
The Inflammatory Feed-Forward Loop Triggered by the Complement Component C3 as a Potential Target in Endometriosis
2021
Copyright © 2021 Agostinis, Zorzet, Balduit, Zito, Mangogna, Macor, Romano, Toffoli, Belmonte, Morello, Martorana, Borelli, Ricci, Kishore and Bulla. The complement system is a major component of humoral innate immunity, acting as a first line of defense against microbes via opsonization and lysis of pathogens. However, novel roles of the complement system in inflammatory and immunological processes, including in cancer, are emerging. Endometriosis (EM), a benign disease characterized by ectopic endometrial implants, shows certain unique features of cancer, such as the capacity to invade surrounding tissues, and in severe cases, metastatic properties. A defective immune surveillance against…
Complement C5 but not C3 is expendable for tissue factor activation by cofactor-independent antiphospholipid antibodies
2018
The complement and coagulation cascades interact at multiple levels in thrombosis and inflammatory diseases. In venous thrombosis, complement factor 3 (C3) is crucial for platelet and tissue factor (TF) procoagulant activation dependent on protein disulfide isomerase (PDI). Furthermore, C5 selectively contributes to the exposure of leukocyte procoagulant phosphatidylserine (PS), which is a prerequisite for rapid activation of monocyte TF and fibrin formation in thrombosis. Here, we show that monoclonal cofactor-independent antiphospholipid antibodies (aPLs) rapidly activate TF on myelomonocytic cells. TF activation is blocked by PDI inhibitor and an anti-TF antibody interfering with PDI bin…
Analysis of complement C3 activation products in human atherosclerotic lesions.
1991
Abstract Cleavage of the complement C3 protein is essential for complement activation. Saline extracts of human atherosclerotic lesions were examined by various techniques for the presence of C3 cleavage fragments. Crossed intermediate gel immunoelectrophoresis revealed that native C3 was the predominate C3 protein in extracts and that the C3dg fragment was also detected. SDS-PAGE/ Western blot analyses of lesion extracts employing monoclonal antibodies directed at C3c and C3dg fragment determinants demonstrated molecular weight bands corresponding to the known molecular weights of all the physiologic C3 cleavage fragments, except Cab which is known to have a short half-life. After C3, the …
Monoclonal antibodies against components of the classical pathway of complement.
1989
Activation of the classical pathway of complement involves several binding and enzymatic cleavage processes. Binding and enzymatic activation results in the appearance of new structures in the individual components. This report describes the different activation steps for C1q, C1r, C1s, C4 and C2 and summarizes monoclonal antibodies reported so far which recognize either conserved epitopes or activation-dependent epitopes with particular emphasis on neoepitopes occurring during the activation cascade.
Is cell salvage safe in liver resection? A pilot study
2007
Abstract Study Objective To investigate the quality of cell salvaged (CS) blood in patients undergoing hemihepatectomy (study group) and compare it with CS-blood from aortic surgery (control group). Design Observational study. Setting Operating room in a university hospital. Measurements 6 patients undergoing hemihepatectomy or aortobifemoral bypass with intraoperative blood loss of more than 800 mL. Samples were drawn from the central venous catheter, from the reservoir of a CS recovery system, and from the processed blood in each patient to determine interleukin (IL)-6, IL-8, IL-10, tumor necrosis factor (TNF), complement C3a, and the terminal complement complex C5b-9. Microbiological ana…
Studies on the mechanism of PMN activation II. by triggering the alternative pathway of complement activation
1982
By means of cobra venom factor (CVF) it is demonstrated that the stimulation of hexosemonophosphate shunt (HMPS) of human polymorphonuclear leukocytes (PMN) by zymosan (Z) and dextran sulfate (DS) is caused by at least two modes of activation: (a) via activation caused by phagocytosis, (b) via activated alternative pathway of complement activation (APC). Active factors of APC presented with phagocytizable objects strongly enhance activation of PMN. The effect of APC can be observed in serum-containing as well as in serum-free cultures. It can be demonstrated that in serum-free cultures the factors of APC participating in the activation of PMN are supplied by monocytes. By the use of synthet…