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Specific Host Restance: The Effector Mechanisms
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Immune adherence brings about the strong attachment of phagocytic leukocytes to parasites. The complement components responsible for immune adherence are and which serve as powerful opsonins. As opsonins, these components are also important for the solubilization and clearance of immune complexes. and also bind to receptors on erythrocytes. The erythrocytes are then cleaned of their attached immune complexes by macrophages in the spleen and liver. Failure to remove these immune complexes can result in their deposition in the kidney glomeruli, a pathological condition in many autoimmune diseases.
Immunologic Mechanisms in Renal Disease
Published in Robin S. Goldstein, Mechanisms of Injury in Renal Disease and Toxicity, 2020
Brian D. Schreiber, Gerald C. Groggel
The classic role for complement in immune injury is the generation of chemotactic factors, particularly C5a, which attract neutrophils to the site of immune deposits (Cochrane et al., 1965). Neutrophils may also be attracted by immune adherence mechanisms involving C3b. The neutrophils then produce injury as discussed later in this chapter. The best examples of complement-neutrophil-mediated glomerulonephritis are the heterologous and autologous phases of anti-GBM nephritis (Cochrane et al., 1965). Depletion of complement in this model prevents neutrophil recruitment and injury (Cochrane et al., 1965). Neutrophil depletion also prevents injury, and repletion of neutrophils produces proteinuria (Henson, 1972). There may be neutrophil-mediated glomerulonephritis without complement as well. Recent work has also shown that complement may be important for the recruitment of platelets to sites of immune deposits.
Biological Functions of Lipopolysaccharide Antibodies
Published in Helmut Brade, Steven M. Opal, Stefanie N. Vogel, David C. Morrison, Endotoxin in Health and Disease, 2020
The human lipid A-specific mAb, HA-IA, has been shown in vitro to augment the serum complement-dependent immune adherence of LPS to human erythrocytes (RBC) and polymorphonuclear leukocytes (PMN) in a dose-dependent manner (44). The binding of immune complexes comprised of HA-IA, LPS, and C’ to RBC and PMN occurs via the classical complement pathway, and this binding takes place through membrane-bound CR1 receptors. It has been hypothesized that mAb HA-IA is capable of reducing the bioavailability of endotoxin in vivo by mediating its binding to and possible clearance by human RBC, acting in conjunction with the reticuloendothelial system or via direct internalization by PMN (44).
Isolation, characterisation and complement fixation activity of acidic polysaccharides from Argemone mexicana used as antimalarials in Mali
Published in Pharmaceutical Biology, 2022
Adama Dénou, Adiaratou Togola, Kari Tvete Inngjerdingen, Nastaran Moussavi, Frode Rise, Yuan Feng Zou, Dalen G. Dafam, Elijah I. Nep, Abubakar Ahmed, Taiwo E. Alemika, Drissa Diallo, Rokia Sanogo, Berit Smestad Paulsen
The complement system cascade is an important part of the innate immune defense. Proteolytic cleavage of complement components by activation of one or more of its three pathways leads to the generation of complement activation products. These mediators exert many biological activities such as the increment of local vascular permeability, the attraction of leucocytes (chemotaxis), immune adherence and modulation of antibody production. Hence, activation of the complement system will contribute to inflammatory responses and immunological defense reactions. The interaction with the complement system by polysaccharides due to fixation could be a good therapeutic strategy for treating inflammatory diseases (Yamada and Kiyohara 1999). Investigation of polysaccharides with complement fixation activity could lead to the discovery of potential immunomodulators.