China
Africa
Explore chapters and articles related to this topic
Morphology, Pathogenesis, Genome Organization, and Replication of Coronavirus (COVID-19)
Published in Hanadi Talal Ahmedah, Muhammad Riaz, Sagheer Ahmed, Marius Alexandru Moga, The Covid-19 Pandemic, 2023
Sadia Javed, Bahzad Ahmad Farhan, Maria Shabbir, Areeba Tahseen, Hanadi Talal Ahmedah, Marius Moga
Ivermectin, an antiparasitic drug, was also recently approved by the FDA to avoid Coronavirus infection following the effective inhibition of in vitro COVID-19 viral replication [159]. The most important component of the human body’s innate defense mechanism, which act as a connection between adaptive and innate immunity, is the complement system, which is made up of more than 35 proteins and regulators. Following the establishment of its function in inflammation and a possible therapeutic impact against some diseases, research on the complement system is advancing quickly [149].
Constitutive Host Resistance
Published in Julius P. Kreier, Infection, Resistance, and Immunity, 2022
Antibodies are components of the inducible immune response and will be considered fully in chapter 7. The complement system is involved in both the constitutive and the inducible systems. The complement system is a group of serum proteins which activate each other sequentially following activation of the initial component by contact with permissible surfaces of microbes or other foreign material, or by contact with immune complexes in the body. When involved in the constitutive defense, complement is activated through the alternate pathway. When involved in the inducible response, activation is through the classical pathway. In the latter case, combination of antibody with the microbe or other target initiates activation of CI; in the former, direct binding of the constitutive serum protein—the complement component C3—with the microbe or other target initiates the process (Figure 3.5).
Immunodeficiency Diseases
Published in Pudupakkam K Vedanthan, Harold S Nelson, Shripad N Agashe, PA Mahesh, Rohit Katial, Textbook of Allergy for the Clinician, 2021
The complement system comprises a tightly regulated pathway that recognizes biochemical divergence between self-structures from structural pathogen associated molecular patterns such as the lipopolysaccharide of gram-negative bacteria, mannose of fungi, ficolins of some gram-positive bacteria. This leads to activation of distinct early complement proteins, generation of convertases that converge on C3 giving rise to the anaphylatoxins C4a and C3a as well as C3b. Beside its opsonic function C3b functions as an enzyme in generating C5a, a chemoattractant for phagocytic cells. Collectively, the anaphylatoxins (C3a, C4a and C5a) mediate the vascular phase of inflammation while C5a recruits the phagocytic cells resulting in integrating the vascular and cellular phase of immune defenses and inflammation. Derangements in this cascade of activating and regulatory proteins leads to either failure of complement mediated defenses and hence recurrent or severe infections or auto activation of complement proteins leading to immune inflammation, defects in complement mediated clearance of apoptotic cells causing autoimmune diseases. Figure 29.2 summarizes the clinical picture as well as the laboratory evaluation of the complement system that leads to a definition of the specific complement protein deficiency.
High level of complement factor Ba within first prenatal test of gestation increases the risk of subsequent gestational diabetes: a propensity score-matched study
Published in Gynecological Endocrinology, 2022
Ying Shen, Junxian Li, Hairong Tian, Ye Ji, Ziyun Li, Junxi Lu, Huijuan Lu, Bo Liu, Fang Liu
In recent years, the innate immune system was shown to be closed related to the metabolic pathway [7]. The complement system is an important part of innate immune system. It can protect host against pathogens and connect innate and adaptive immune response [8]. Abnormal regulation of complement system or deficiency of complement can increase the susceptibility of chronic inflammatory diseases and infections [9]. The complement cascades are activated in three different ways: the classical pathway, the alternative pathway and the mannose binding lectin way. Among them, the alternative pathway has attracted much more attention because of its potential role in metabolic diseases such as hypertension, type 2 diabetes mellitus, as well as dyslipidemia, and CFB is critical for its activation [10–12]. CFB is a single chain glycoprotein, which consists of five protein domains. After the alternative pathway of complement system was activated, factor B was cleaved into two fragments, Ba and Bb. The molecular weight of Ba fragment is about 30,000 dalton, which is composed of 234 amino acids and comes from the N-terminal part of the precursor molecule of factor B [13,14].
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.
Levels of lymphocyte-associated regulators of complement system CD55 and CD59 are changed in schizophrenia patients
Published in International Journal of Psychiatry in Clinical Practice, 2021
Alper Togay, Bilge Togay, Deniz Ozbay Gediz, Sadıka Halide Akbaş, Sadi Köksoy
The complement system is activated via three pathways known as classical, alternative and lectin pathways. Complement triggers three immune functions: 1-phagocytosis, by opsonising antigens; 2-inflammation, by attracting macrophages and neutrophils; 3-membrane attack, by rupturing cell wall of bacteria (Abbas and Lichtman 2009). The complement system is regulated by complement regulatory proteins. There are three major human cell surface regulatory proteins. The first one is CD46 (membrane cofactor protein), which facilitates the inactivation of C3b and C4b (Kawano et al. 1999); the second one is CD59, which is an inhibitor that binds to C8 and C9 to prevent the assembly of the membrane attack complex (Kimberley et al. 2007); and the third one is CD55, also known as ‘decay accelerating factor (DAF)’, which accelerates the removal of preformed C3 and C5 convertases from the cell surface (Christmas et al. 2006). These complement regulatory proteins are at a higher concentration in the blood plasma than the complement proteins.