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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.
The maternal immune system during pregnancy
Published in Hung N. Winn, Frank A. Chervenak, Roberto Romero, Clinical Maternal-Fetal Medicine Online, 2021
Complement is a collection of serum proteins that bind pathogens, leading to immediate destruction, opsonization, or chemotaxis. Once activated, factors remain bound to the pathogen (i.e., factor C3b) or released locally for neutrophil chemotaxis (i.e., factor C3a). Complement is activated through multiple mechanisms resulting in the formation of a “C3 convertase” (Fig. 1): (i) it is activated by antibodies present on pathogens through factor C1q (the “classical” pathway); (ii) it binds directly to the pathogen through factor C3b (the “alternative” pathway), or (iii) it is activated by the terminal mannose of bacterial N-acetyl glucosamine through mannose-binding protein (the “lectin” pathway). The presence of C3b then opsonizes organisms for phagocytosis by neutrophils and macrophages. In some cases, such as with Neisseria sp., complement also forms a multicomponent membrane attack complex (MAC) that leads to direct perforation and lysis of the organism (9,10).
The cell and tissues
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Complement is an intriguing group of proteins, that come together to help activate the immune system. It is also responsible for labelling invading microorganisms, to facilitate their destruction by the phagocytic neutrophils and macrophages.
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
Potential Treponema denticola-based periodontal vaccine to resolve a global public health challenge: a narrative literature review
Published in Expert Review of Vaccines, 2022
Navid Mirmohammadsadegh, Neshaut Mashreghi Mohammadi, Mohsen Amin
The habitat of periodontal pathogens are bathed in gingival crevicular fluid (GCF), which is rich in innate immune system effectors [73,74]. The complement participates in clearing microbes and altering host cells and compromise a vital link between the innate and adaptive immune system [75]. Although complement activity is essential for immune homeostasis, dysregulation of complement response exerts harmful effects on the host cells [76]. In this context, Factor H (FH) is 150 kDa glycoprotein which is available as soluble or membrane-bound form in the human body. FH negatively regulates the complement system; thus, FH protects host cells from the activated complement [76]. Intriguingly, T. denticola can evade complement-mediated killing by bounding to complement FH. Mechanistically, T. denticola attaches to FH by factor H binding protein B (FhbB) and cleaves FH via dentilisin, thereby altering complement-mediated responses [77].
Lupus manifestations in children with primary immunodeficiency diseases: Comprehensive phenotypic and genetic features and outcome
Published in Modern Rheumatology, 2021
Sulaiman M. Al-Mayouf, Hajar A. Alreefi, Tuqa A. Alsinan, Ghada AlSalmi, Abdulaziz AlRowais, Waleed Al-Herz, Anas M. Alazami, Abdullah Alsonbul, Hamoud Al-Mousa
Clinical and genetic characteristics of complement deficient patients are shown in Table 3. Twenty-six patients were C1q deficient. All patients had undetectable serum C1q levels, while 11 patients underwent molecular genetic testing and proved to have C1q pathogenic mutations. All patients had an early onset of lupus manifestations; 16 patients (61.5%) developed the symptoms prior their fifth birthday. Interestingly, there was a prominent family history of SLE; 15 patients belonging to seven consanguineous families. Twenty-five patients had recurrent mucocutaneous lesions, including oral ulceration, discoid rash and scarring alopecia and yellowish dystrophic nails. Major organ involvement was common; nine patients had biopsy proven nephritis; seven patients had proliferative glomerulonephritis and two patients had membranoproliferative glomerulonephritis as per the ISN/RPS classification [15]. In addition, six patients had chronic lung infiltrations with restricted lung disease proven by pulmonary function test. Five patients had neurological manifestation in form of spastic diplegia, and brain magnetic resonance imaging (MRI) showed basal ganglia calcification, and one patient had transverse myelitis. However, one patient with C1q deficiency proven by genetic testing was asymptomatic, but laboratory results revealed high inflammatory markers and high ANA and anti-SSA/Ro and anti-La/SSB antibodies. Also, he had elevated thyroid stimulating hormone (TSH) and low free thyroxine (T4) with positive anti-thyroglobulin antibodies, which are consistent with autoimmune hypothyroidism.