Complement system proteins which interact with C3b or C4b A superfamily of structurally related proteins

1986 ◽  
Vol 7 (7-8) ◽  
pp. 230-234 ◽  
Author(s):  
K.B.M. Reid ◽  
D.R. Bentley ◽  
R.D. Campbell ◽  
L.P. Chung ◽  
R.B. Sim ◽  
...  
Keyword(s):  
Complement System ◽  
Complement System Proteins ◽  
Related Proteins

Molecular Mechanisms of Complement System Proteins and Matrix Metalloproteinases in the Pathogenesis of Age-Related Macular Degeneration

2019 ◽  
Vol 19 (10) ◽  
pp. 705-718 ◽  
Author(s):  
Naima Mansoor ◽  
Fazli Wahid ◽  
Maleeha Azam ◽  
Khadim Shah ◽  
Anneke I. den Hollander ◽  
...  
Keyword(s):  
Matrix Metalloproteinases ◽  
Macular Degeneration ◽  
Complement System ◽  
Molecular Mechanisms ◽  
Critical Role ◽  
Age Related Macular Degeneration ◽  
Genetic Changes ◽  
Complement System Proteins ◽  
Age Related ◽  
Common Genetic Variants

: Age-related macular degeneration (AMD) is an eye disorder affecting predominantly the older people above the age of 50 years in which the macular region of the retina deteriorates, resulting in the loss of central vision. The key factors associated with the pathogenesis of AMD are age, smoking, dietary, and genetic risk factors. There are few associated and plausible genes involved in AMD pathogenesis. Common genetic variants (with a minor allele frequency of >5% in the population) near the complement genes explain 40–60% of the heritability of AMD. The complement system is a group of proteins that work together to destroy foreign invaders, trigger inflammation, and remove debris from cells and tissues. Genetic changes in and around several complement system genes, including the CFH, contribute to the formation of drusen and progression of AMD. Similarly, Matrix metalloproteinases (MMPs) that are normally involved in tissue remodeling also play a critical role in the pathogenesis of AMD. MMPs are involved in the degradation of cell debris and lipid deposits beneath retina but with age their functions get affected and result in the drusen formation, succeeding to macular degeneration. In this review, AMD pathology, existing knowledge about the normal and pathological role of complement system proteins and MMPs in the eye is reviewed. The scattered data of complement system proteins, MMPs, drusenogenesis, and lipofusogenesis have been gathered and discussed in detail. This might add new dimensions to the understanding of molecular mechanisms of AMD pathophysiology and might help in finding new therapeutic options for AMD.

scholarly journals Systems Biology Modeling of the Complement System Under Immune Susceptible Pathogens

2021 ◽  
Vol 9 ◽  
Author(s):  
Nehemiah T. Zewde ◽  
Rohaine V. Hsu ◽  
Dimitrios Morikis ◽  
Giulia Palermo
Keyword(s):  
Complement System ◽  
Membrane Attack Complex ◽  
Factor H ◽  
Immunoglobulin M ◽  
The Body ◽  
Complement Components ◽  
Invasive Pathogens ◽  
Time Profiles ◽  
Related Proteins ◽  
The Complement System

The complement system is assembled from a network of proteins that function to bring about the first line of defense of the body against invading pathogens. However, complement deficiencies or invasive pathogens can hijack complement to subsequently increase susceptibility of the body to infections. Moreover, invasive pathogens are increasingly becoming resistant to the currently available therapies. Hence, it is important to gain insights into the highly dynamic interaction between complement and invading microbes in the frontlines of immunity. Here, we developed a mathematical model of the complement system composed of 670 ordinary differential equations with 328 kinetic parameters, which describes all three complement pathways (alternative, classical, and lectin) and includes description of mannose-binding lectin, collectins, ficolins, factor H-related proteins, immunoglobulin M, and pentraxins. Additionally, we incorporate two pathogens: (type 1) complement susceptible pathogen and (type 2) Neisseria meningitidis located in either nasopharynx or bloodstream. In both cases, we generate time profiles of the pathogen surface occupied by complement components and the membrane attack complex (MAC). Our model shows both pathogen types in bloodstream are saturated by complement proteins, whereas MACs occupy <<1.0% of the pathogen surface. Conversely, the MAC production in nasopharynx occupies about 1.5–10% of the total N. meningitidis surface, thus making nasal MAC levels at least about eight orders of magnitude higher. Altogether, we predict complement-imbalance, favoring overactivation, is associated with nasopharynx homeostasis. Conversely, orientating toward complement-balance may cause disruption to the nasopharynx homeostasis. Thus, for sporadic meningococcal disease, our model predicts rising nasal levels of complement regulators as early infection biomarkers.

Acquired coagulopathy and complement system pathology in chronic hepatic disorders.

2021 ◽  
Author(s):  
Е.Ю. Коновалова ◽  
М.В. Преснякова
Keyword(s):  
Immune Response ◽  
Innate Immune Response ◽  
Complement System ◽  
Clinical Picture ◽  
Coagulation Factors ◽  
Innate Immune ◽  
Complement System Proteins ◽  
Hepatic Diseases ◽  
System Components

Комплемент и коагуляция являются эволюционно связанными протеолитическими гуморальными системами, которые имеют решающее значение для осуществления врожденного иммунного ответа на повреждение и инфекцию, ограничения кровотечения и патологического тромбообразования. Печень играет центральную роль в функционировании системы гемостаза и комплемента: она синтезирует большинство факторов свертывания и их ингибиторов, а также протеины системы комплимента. При хронических заболеваниях печени нарушения системы гемостаза протекают по типу коагулопатий, выраженность которых будет определять клиническую картину основного заболевания. В обзоре представлены данные о роли сосудисто-тромбоцитарного, коагуляционного, антикоагулянтного и фибринолитического звеньев системы гемостаза и компонентов системы комплемента в патогенезе хронических заболеваний печени. Complement and coagulation are evolutionarily related proteolytic humoral systems that are crucial for the innate immune response to injury and infection, for limiting hemorrhage and pathological thrombosis. The liver plays a central role in the functioning of hemostasis and complement system. It synthesizes most coagulation factors and their inhibitors, as well as complement system proteins. In chronic hepatic diseases, hemostasis disorders proceed as coagulopathies, and their severity determine the clinical picture of basic disease. This review presents data about the role of vascular-platelet, coagulant, anticoagulant and fibrinolytic links of hemostasis and complement system components in the pathogenesis of chronic hepatic diseases.

scholarly journals AFM study of complement system assembly initiated by antigen-antibody complex

2006 ◽  
Vol 4 (1) ◽  
pp. 194-206 ◽  
Author(s):  
Almira Ramanaviciene ◽  
Valentinas Snitka ◽  
Rasa Mieliauskiene ◽  
Rolandas Kazlauskas ◽  
Arunas Ramanavicius
Keyword(s):  
Complement System ◽  
Self Assembly ◽  
Substrate Surface ◽  
Leukemia Virus ◽  
Complement System Proteins ◽  
Sio2 Substrate ◽  
Force Microscopy ◽  
Highly Active ◽  
Antibody Complex ◽  
Antigen Antibody

AbstractThe shape and size of complement system C1 components assembled on a SiO2 surface after classical activation by antigen-antibody complex was determined by tapping mode atomic force microscopy (AFM). The SiO2 substrate was silanized and bovine leukemia virus proteins gp51 were covalently bound to the SiO2 substrate. Self-assembly of complement system proteins was investigated by AFM. Uniform coating of silanized surface by gp51 proteins was observed by AFM. After incubation of gp51 coated substrate in anti-gp51 antibody containing solution, Ag-Ab complexes were detected on the substrate surface by AFM. Then after treatment of Ag-Ab complex modified substrate by guinea-pig blood serum containing highly active complement system proteins for 3 minutes and 30 minutes features 2–3 times and 5–8 times higher in diameter and in height if compared with those observed after formation of Ag-Ab complex, were observed respectively on the surface of SiO2. This study revealed that AFM might be applied for the imaging of complement system assembly and provides valuable information that can be used to complement other well-established techniques.

scholarly journals Proteomic Analysis of Human Serum from Patients with Chronic Kidney Disease

Biomolecules ◽  
2020 ◽  
Vol 10 (2) ◽  
pp. 257 ◽  
Author(s):  
Yulia Romanova ◽  
Alexander Laikov ◽  
Maria Markelova ◽  
Rania Khadiullina ◽  
Alfiz Makseev ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Complement System ◽  
Multiple Reaction Monitoring ◽  
Public Health Problem ◽  
P Value ◽  
Important Public Health Problem ◽  
Ki 67 ◽  
Complement System Proteins ◽  
Cytokines And Chemokines

Chronic kidney disease (CKD) is an important public health problem in the world. The aim of our research was to identify novel potential serum biomarkers of renal injury. ELISA assay showed that cytokines and chemokines IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-9, IL-10, IL-12 (p70), IL-13, IL-15, IL-17, Eotaxin, FGFb, G-CSF, GM-CSF, IP-10, MCP-1, MIP-1α, MIP-1β, PDGF-1bb, RANTES, TNF-α and VEGF were significantly higher (R > 0.6, p value < 0.05) in the serum of patients with CKD compared to healthy subjects, and they were positively correlated with well-established markers (urea and creatinine). The multiple reaction monitoring (MRM) quantification method revealed that levels of HSP90B2, AAT, IGSF22, CUL5, PKCE, APOA4, APOE, APOA1, CCDC171, CCDC43, VIL1, Antigen KI-67, NKRF, APPBP2, CAPRI and most complement system proteins were increased in serum of CKD patients compared to the healthy group. Among complement system proteins, the C8G subunit was significantly decreased three-fold in patients with CKD. However, only AAT and HSP90B2 were positively correlated with well-established markers and, therefore, could be proposed as potential biomarkers for CKD.

scholarly journals Complement-Related Proteins and Their Measurements: The Current Status of Clinical Investigation

Nephron ◽  
2020 ◽  
pp. 1-6
Author(s):  
Katsuki Ohtani
Keyword(s):  
Complement System ◽  
Inflammatory Diseases ◽  
Clinical Investigation ◽  
Pathological Condition ◽  
Current Status ◽  
Complement Factor ◽  
Complement Factors ◽  
Foreign Countries ◽  
Autoimmune And Inflammatory Diseases ◽  
Related Proteins

Complement has been considered to be a factor that protects the host against invading microorganisms during infection. However, in recent years, complement-related protein deficiency has been found to be involved in the onset of various diseases, such as autoimmune and inflammatory diseases. In Japan, C3, C4, and CH50 tests were generally performed only when a complement system examination was necessary and there were not enough examinations for other complement factors. Since the complement system has a very complicated activation pathway, at present, it is not well known which molecule must be measured to understand the pathological condition or pathogenesis in complement-related diseases. Furthermore, since the frequency of complement factor gene alleles also differs depending on race, data from foreign countries cannot be directly applied to Japanese populations. Under these circumstances, the Japanese Association for Complement Research (JACR) has prepared approximately 20 items for complement-related examinations, including the 5 categories of functional analysis, complement factors, complement regulators, activation products, and autoantibodies.

Regulation of plaque size and host range by a vaccinia virus gene related to complement system proteins

Virology ◽  
1991 ◽  
Vol 181 (1) ◽  
pp. 158-164 ◽  
Author(s):  
Fukumi Takahashi-Nishimaki ◽  
Shin-Ichi Funahashi ◽  
Keizaburo Miki ◽  
So Hashizume ◽  
Masanobu Sugimoto
Keyword(s):  
Vaccinia Virus ◽  
Host Range ◽  
Complement System ◽  
Plaque Size ◽  
Complement System Proteins ◽  
Virus Gene

scholarly journals EPIGENOMIC FACTORS FOR THE DEVELOPMENT OF PERITONEAL ADHESIONS

2020 ◽  
pp. 30-34
Author(s):  
V. V. Boyko ◽  
D. O. Yevtushenko ◽  
I. V. Kryvorotko ◽  
I. A. Taraban ◽  
D. V. Minukhin ◽  
...  
Keyword(s):  
Acute Phase ◽  
Adhesion Molecule ◽  
Complement System ◽  
Comparison Group ◽  
Acute Phase Proteins ◽  
C Reactive Protein ◽  
Complement System Proteins ◽  
Factors Associated ◽  
Reactive Protein ◽  
The Complement System

Summary. The etiology of the development of adhesive disease — the most common postoperative complication — can be determined by epigenomic disorders related to various links of resistance and immunogenetic control. Purpose of the study. To study the epigenomic factors in the development of adhesive disease, the immune status of patients operated on in the abdominal cavity was studied. The comparison group included 55 patients with a complicated course of peritoneal commissural disease, the main group consisted of 59 patients operated on on the abdominal organs on the background of peritoneal commissural disease, the course of which was asymptomatic. Results and its discussion. The revealed epigenomic factors associated with the risk of developing adhesive disease: belongs to an increase in the concentration of acute phase proteins - ceruloplasmin, haptoglobin, C-reactive protein, C3 fragment of the complement system proteins, changes in the expression of adhesion molecule genes (CD31 increased by 10 %, CD54 increased to 24.1 % in comparison with the comparison group — 13.25 %). Conclusions. The results of our studies showed that patients with adhesive disease have a wide range of epigenome trigger factors. Epigenomic factors associated with the risk of developing adhesive disease include an increase in the concentration of acute phase proteins - ceruloplasmin, haptoglobin, C-reactive protein, C3 fragment of the complement system proteins, changes in the expression of adhesion molecule genes (CD31 increased by 10 %, CD54 increased to 24, 1 % compared with the comparison group - 13.25 %)

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