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Specific Host Restance: The Effector Mechanisms
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
The complement components, designated by a capital C, are all proteins. They comprise ten percent of total human serum protein. Each component is identified by a numbered suffix, C1, C2, etc., that reflects the order in which they were originally purified rather than the order in which they react. Additional serum proteins called factors B, D, and P (properdin) are also involved in complement activation. The complement components circulate in the blood in inactive form. During the activation process, they may change in conformation, undergo proteolytic cleavage, or aggregate into multisubunit proteins. By convention, when a complement protein is split in two, the fragments are designated by a lower case a (for the smaller piece) and b (for the larger piece). The activation mechanisms can generate a protein with an enzymatic site or a binding site not exposed on the inactive component. The sites generated enable each component to react with the next component in the cascade. Activated complement proteins have biological activities that play a variety of roles in eliminating the invading microbe. In the classical pathway, factors B and D and properdin (P) amplify reactions after they have been initiated. For this reason, the classical pathway is sometimes known as the properdin pathway.
Inherited Defects in Immune Defenses Leading to Pulmonary Disease
Published in Stephen D. Litwin, Genetic Determinants of Pulmonary Disease, 2020
Two pathways of complement activation are known, the classical and alternate pathways. Enhancement of phagocytosis of encapsulated pneumococci by serum requires not only specific antibody but also C3 [20]; maximal enhancement occurs when the alternate pathway is involved. Endotoxin-coated particles in an emulsion are only phagocytized via the alternate pathway without antibody involvement [21].
The Acute Phase Complement Proteins
Published in Andrzej Mackiewicz, Irving Kushner, Heinz Baumann, Acute Phase Proteins, 2020
The C3 protein is a principle source of biologically active cleavage products that mediate inflammation, solubilize and clear immune complexes, and further propogate the complement cascade, resulting in assembly of the terminal complement protein complex (the membrane attack complex, MAC) and cytolysis via the generation of discrete membrane channels. The complement effector proteins are controlled by an elaborate network of regulatory proteins, some of which also serve as cell-surface receptors for complement activation products. A detailed account of the complement effector and regulatory genes and gene products is beyond the scope of this chapter. The reader should consult relatively recent reviews.9-11
Association of serum mannose-binding lectin, anti-phospholipase A2 receptor antibody and renal outcomes in idiopathic membranous nephropathy and atypical membranous nephropathy: a single center retrospective cohort study
Published in Renal Failure, 2022
Yuchao Zhao, Meishun Cai, Zhenbin Jiang, Bao Dong, Yu Yan, Yina Wang, Li Zuo
Membranous nephropathy (MN) is the most common cause of nephrotic syndrome in adults and can be grouped into idiopathic membranous nephropathy (iMN) without identified causes and secondary membranous nephropathy (sMN), which is secondary to immune disease, infection, tumors, or any other cause [1]. The renal pathology of iMN is characterized by the deposition of subepithelial immune deposits that consist mainly of immunoglobulin (Ig) G and complement [2], indicating that the complement system plays a substantial role in iMN. Atypical membranous nephropathy (aMN) is a new type of membranous nephropathy characterized by cells proliferation, multi-site immune complex deposition, most of patients showed ‘full house’ in immunofluorescence, including IgA, IgG, IgM, C3, C1q positive, but no clinical evidence of a secondary cause, also called ‘lupus-like’ membranous nephropathy or ‘full-house’ membranous nephropathy [3,4]. It is controversial whether this is a new type of membranous nephropathy or an early form of secondary membranous nephropathy. From 2006 to 2015, aMN accounted for 44.39% (364 cases) of membranous nephropathy cases (820 cases) out of 3210 cases of renal puncture in our previous study [3]. The deposition of a variety of immune complexes and complement indicates that complement activation may play a role in its onset.
The Complement System in Retinal Detachment with Choroidal Detachment
Published in Current Eye Research, 2022
Shasha Luo, Yanghao Chen, Lufei Yang, Xuechun Gong, Zhifeng Wu
The complement system plays a crucial role in the host's defense against infection and in regulating immune and inflammatory responses.3 Complement activation can be achieved through three distinct pathways: the classical pathway, the alternative pathway, and the lectin pathway. Complement activation results in the production of several biologically active molecules such as complement C3a, complement C5a, and the membrane attack complex (MAC). These molecules eliminate the foreign cells, bacteria, and viruses, but persistent inflammatory responses can injure host cells.4 Interestingly, a chronically low level of complement activation is always present in normally functioning eyes. This phenomenon is attributed to the presence of complement regulatory proteins (CRegs) that strictly control complement activation, so that the biological activity of complement proteins is directed against foreign factors rather than the host's own tissue.5
A Differential Immune Modulating Role of Vitamin D in Urinary Tract Infection.
Published in Immunological Investigations, 2022
The complement activation is thought to be capable of linking both the innate and humoral immunity to induce protection against microbial insult. The results obtained from this study showed that although serum C3 levels in the patient group were higher than that of the control group and had a significant association with 25(OH)D levels (r = 0.404, P = .025), the C4 levels did not differ significantly between the two groups and show such an association with 25(OH)D levels (Figure 2). In the control group, a statistically negative correlation was found between the levels of C3 and 25(OH)D (r = –0.285, P = .022) while the C4 levels were positively correlated with serum 25(OH)D levels (r = 0.309, P = .017). The assessment of the hemolytic activity of the alternative pathway (AP50) was found to be increased in the patient group, but not the classical pathway (CH50) (Figure 3). In addition, the statistical level was insignificant for the association of CH50 and AP50 with 25(OH)D levels. Similarly, the findings showed no significant correlations for both AP50 and CH50 in controls. Further analyses indicated that although sufficient 25(OH)D status partly alters the production level of C3 complement component, the functional activity of complement pathways remains unchanged (Table 2). This provides a suggestion regarding a possible promoted phagocytosis of opsonized bacteria and maintenance of the level of the complement activation through the alternative pathway.