China
Africa
Explore chapters and articles related to this topic
Specific Host Restance: The Effector Mechanisms
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
The membrane attack complex usually enters the membranes of cells to which antibody is bound. A few of these complexes, however, may detach from the antibody-coated cell on which they formed and deposit on adjacent cells, resulting in the loss of healthy host cells in the vicinity. When this occurs it is referred to as a bystander effect of complement activation.
Immune system and Innate Immunity
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The activation of C3 is a central event of both classical and alternative pathways leading to the formation of C5 convertases that initiate the terminal (membrane attack) sequence. The classical pathway (initiated by immunoglobulin G (IgG) or immunoglobulin M (IgM) antigen–antibody complexes) and the alternative pathway (initiated by liposaccharide, endotoxin or immunoglobulin A [IgA]) produce complement C3, which cleaves C5 into C5a and C5b. The formed C5b combines with C6, C7, C8 and C9 to produce the membrane attack complex (MAC) that damages cell membranes (Figure 55.2). The classical pathway is shown in Figure 55.2.
The Immune System and its Function
Published in Istvan Berczi, Pituitary Function and Immunity, 2019
The complement system48,49 comprises at least 13 different plasma proteins, which play an important role in immunological and nonimmunological host defense. The immunological defense system involves nine proteins (C1, C2, C3, C4, C5, C6, C7, C8, C9) that execute the complement reaction according to the so-called classical pathway. IgM and IgG (with the exception of IgG4 antibodies) expose a receptor site on their Fc portion for complement, after combination with the specific antigen. This receptor is recognized by the first complement component, which is followed by the activation of C4, C2, C3, and C5, by enzymatic cleavage, each component is being a pro-enzyme that can act on a number of molecules of the next component in the system after activation. Once C5 is cleaved to C5a and C5b, C5b initiates the membrane attack complex that is a self-assembling process, involving the remaining complement components. Apparently, certain peptides of the C5b, 6, 7, 8, and 9 complex are inserted during this process into the phospholipid bilayer of the membrane, so as to form a channel of about 55 to 100 Å in diameter, which allows the escape of cytoplasmic components leading to cell death.
Retinal findings in glomerulonephritis
Published in Clinical and Experimental Optometry, 2022
Heather G Mack, Deborah J Colville, Phillip Harraka, Judith Anne Savige, Alessandro Invernizzi, Samantha Fraser-Bell
The classical pathway is typically ‘antibody-dependent’ and activated by IgM-IgG clusters. The lectin pathway primarily recognises carbohydrate patterns on microbial surfaces. The alternative pathway is activated by bacteria and bacterial toxins, but in contrast to the classical and lectin pathways, has a low basal rate of turnover (‘tick over’) that is thought to monitor for pathogen invasion. In further contrast to the classical and lectin pathways, the activated alternative pathway can also bind host cells, but this is usually controlled by an army of membrane-expressed or fluid phase-recruited complement regulators. The common terminal pathway, shared by all three pathways, comprises factors C5 to C9. When C5b associates with C6 and C7, the complex is inserted into the cell membranes and interacts with C8, inducing binding of C9 to form a lytic pore (membrane attack complex, or terminal complement complex), the hallmark of complement attack.1,2
Importance of mannose-binding lectin2 polymorphism (rs1800450) in infections in children
Published in Biomarkers, 2022
Metin Uysalol, Suheyla Gumus, Raif Yildiz, Ezgi Pasli Uysalol, Sacide Pehlivan, Mustafa Pehlivan, Istemi Serin
The complement system is activated by three main pathways: the classical, the lectin pathway, or the alternative pathway (AP) (Thiel 2007, Cedzynski et al.2012). Although they are each initiated differently, all result in activation of C3 and C5 and formation of the membrane attack complex (MAC, C5b-9), which binds to the target. MBL is a factor associated with the lectin pathway as a member of collectins (Thiel 2007, Cedzynski et al.2012). Despite direct lysis of the pathogen through complement activation, these factors act as opsonins and thus contribute to phagocytosis (Thiel 2007, Cedzynski et al.2012). MBL, which is an important factor against respiratory pathogens with this key role, is also an important research topic with the clinical effects of gene polymorphisms in infections in children.
Complement system network in cell physiology and in human diseases
Published in International Reviews of Immunology, 2021
Roberta Romano, Giuliana Giardino, Emilia Cirillo, Rosaria Prencipe, Claudio Pignata
The classical pathway is initiated by the interaction of immune complexes, made of the Fc portion of IgM or IgG and antigens, with the first zymogen of the cascade, C1q which, in resting conditions, forms an inactive complex with C1r and C1s. Upon interaction with immune complexes, C1q activates C1r, which, in turn, cleaves and activates C1s (Figure 1A). This induces the cleavage of two other components, C2 and C4, with the formation of the complex C4b2a, which hydrolyzes C3 into C3a and C3b that, respectively, recruits inflammatory cells and binds to the C4b2a complex forming C5 convertase [10]. The latter is responsible for the formation of the Membrane Attack Complex that induces lysis of bacterial membranes inserting functional pores in it [1]. Also, viral proteins, apoptotic cells and C-reactive protein can trigger this pathway independently of the presence of antibodies.