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Anatomical and Physiological Changes in Pregnancy
Published in Karl H. Pang, Nadir I. Osman, James W.F. Catto, Christopher R. Chapple, Basic Urological Sciences, 2021
Joanna Shepherd, Stephen Radley
CD55 complement regulator protects the foetus from maternal complement injury.Expression is increased by progesterone.CD55 is favourable for DR E. coli colonisation.
Immune function of epithelial cells
Published in Phillip D. Smith, Richard S. Blumberg, Thomas T. MacDonald, Principles of Mucosal Immunology, 2020
Richard S. Blumberg, Wayne Lencer, Arthur Kaser, Jerrold R. Turner
The intestinal epithelium constitutively secretes, or is induced to secrete, inflammatory mediators and, upon recognition of microbial components such as microbe-associated molecular patterns, a variety of host-protective soluble factors. These include those with antimicrobial activity, such as lactoferrin, lysozyme, peroxidase, cathelicidin, α-defensins, and β-defensins, which are largely provided by epithelial cells (β-defensins) and Paneth cells (α-defensins). These factors serve to regulate the composition of the commensal microbiota and protect the host from pathogenic invasion. The secretion of antimicrobial peptides is a major common property of all body surfaces. Epithelial cells also secrete a variety of different complement components into the lumen; consistent with this, epithelial cells express CD55 (decay accelerating factor), which protects the epithelium from inappropriate complement deposition. In other regions of the intestinal tract, a variety of other nonspecific factors serve a role in host defense, such as gastric acid from the stomach, bile salts from the biliary system, and urea in the urogenital system.
The complement system in health and disease
Published in Gabriel Virella, Medical Immunology, 2019
Decay-accelerating factor (DAF, CD55) is a complement-inhibitory protein widely expressed on host cell membranes. The name of this factor derives from the fact that it can accelerate the dissociation of active C4b2a complexes, turning off their ability to continue activating C3. In addition, DAF attaches to membrane-bound C4b and C3b and prevents the subsequent interaction of C4b with C2 and of C3b with factor B, respectively. As a consequence, the two types of C3 convertases, C4b2a and C3bBb, will not be formed or will become dissociated, and the rate of additional C3 activation is significantly limited. Thus, the host cell will be spared from complement-mediated membrane damage.
The role of the alternative pathway in paroxysmal nocturnal hemoglobinuria and emerging treatments
Published in Expert Review of Clinical Pharmacology, 2022
Jong Wook Lee, Robert A. Brodsky, Jun-Ichi Nishimura, Austin G. Kulasekararaj
Under normal physiologic conditions, complement activity is tightly controlled by complement regulators that protect the host against complement-mediated injury [3,21,22]. Membrane-bound complement regulators include, among others, CD55 (decay accelerating factor) and CD59 (membrane inhibitor of reactive lysis). CD55 inhibits the formation and stability of C3 and C5 convertases and thus limits the ability of C3 convertases to promote further complement activation, whereas CD59 prevents assembly of the MAC (C5b-9). The Inab phenotype, which indicates a genetic defect in CD55 on the erythrocyte membrane, shows no hemolytic findings [26]. On the other hand, the genetic deficiency of CD59 has the same hemolytic findings and symptoms as PNH [27]. These results suggest that the deficiency of CD59 is particularly important for the hemolytic mechanism of PNH. PNH cells can be further subdivided into type 2 (mutation causing a partial GPI defect) and type 3 (mutation causing a complete GPI defect) GPI-deficient clones [28]. Type 3 cells have been associated with higher LDH levels and greater hemolytic activity [28].
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.
Safety of current treatments for paroxysmal nocturnal hemoglobinuria
Published in Expert Opinion on Drug Safety, 2021
Paroxysmal nocturnal hemoglobinuria (PNH) is a rare, progressive, and life-threatening hematopoietic stem cell disorder whose clinical manifestations include intravascular hemolysis, thrombosis, and bone marrow failure [1]. The disease arises as a consequence of a somatic mutation in the phosphatidylinositol glycan class A (PIG-A) gene that prevents synthesis of N-acetyl-D-glucosamine phosphatidylinositol, an essential component of glycosylphosphatidylinositol anchor protein (GPI-AP) [2]. Deficiency of GPI-anchored complement-inhibitor proteins, especially CD55 (decay-accelerating factor) and CD59 (membrane inhibitor of reactive lysis), causes chronic intravascular hemolysis, a hallmark clinical manifestation of PNH that is mediated by the alternative pathway of complement (APC). The APC cascade can be divided into amplification of the C3 and C5 convertases and the cytolytic membrane attack complex (MAC). CD55 regulates the formation and stability of the C3 and C5 convertases, and CD59 blocks the formation of the MAC [3]. Chronic hemolysis leads to release of free hemoglobin, which causes nitric oxide depletion, reactive oxygen species increases, endothelial dysfunction, and platelet and monocyte activation [4,5]. Consequently, PNH is typically characterized by thrombosis and organ damage, as well as severe hemolytic anemia, and symptoms include hemoglobinuria, severe fatigue, abdominal pain, dysphagia, erectile dysfunction, renal dysfunction, and pulmonary hypertension [6,7]. Despite best supportive care, PNH is associated with high morbidity and mortality [6,8–10].