scholarly journals Importance the Type 1 (CR1) and Type 3 (CR3) Complement Receptors in the Infectious Disease

2021 ◽  
Vol 2 (3) ◽  
pp. 216-217
Author(s):  
Cassio Marinho Campelo
Keyword(s):  
Infectious Disease ◽  
Complement System ◽  
Enzymatic Reactions ◽  
Complement Receptors ◽  
Defence Mechanisms ◽  
Effector Functions ◽  
Type 3 ◽  
The Complement System

The complement system is one of the host’s primary defence mechanisms against pathogens. Its activation involves proteolytic cascades of enzymatic reactions that result in products with effector functions and recognition of molecules on the surface of microorganisms [1,2].

scholarly journals Fcγand Complement Receptors and Complement Proteins in Neutrophil Activation in Rheumatoid Arthritis: Contribution to Pathogenesis and Progression and Modulation by Natural Products

2015 ◽  
Vol 2015 ◽  
pp. 1-22 ◽  
Author(s):  
Adriana Balbina Paoliello-Paschoalato ◽  
Larissa Fávaro Marchi ◽  
Micássio Fernandes de Andrade ◽  
Luciana Mariko Kabeya ◽  
Eduardo Antônio Donadi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Complement System ◽  
Proteolytic Enzymes ◽  
Joint Damage ◽  
Complement Receptors ◽  
Effector Functions ◽  
Extracellular Traps ◽  
Persistent Inflammation ◽  
The Complement System ◽  
Frustrated Phagocytosis

Rheumatoid arthritis (RA) is a highly disabling disease that affects all structures of the joint and significantly impacts on morbidity and mortality in RA patients. RA is characterized by persistent inflammation of the synovial membrane lining the joint associated with infiltration of immune cells. Eighty to 90% of the leukocytes infiltrating the synovia are neutrophils. The specific role that neutrophils play in the onset of RA is not clear, but recent studies have evidenced that they have an important participation in joint damage and disease progression through the release of proteolytic enzymes, reactive oxygen species (ROS), cytokines, and neutrophil extracellular traps, in particular during frustrated phagocytosis of immune complexes (ICs). In addition, the local and systemic activation of the complement system contributes to the pathogenesis of RA and other IC-mediated diseases. This review discusses (i) the participation of Fcγand complement receptors in mediating the effector functions of neutrophils in RA; (ii) the contribution of the complement system and ROS-dependent and ROS-independent mechanisms to joint damage in RA; and (iii) the use of plant extracts, dietary compounds, and isolated natural compounds in the treatment of RA, focusing on modulation of the effector functions of neutrophils and the complement system activity and/or activation.

Modulation in the expression of type 1 (CR1/CD35) and type 3 (CR3/CD11b) complement receptors on leukocytes from patients with Visceral leishmaniasis

2020 ◽  
Vol 218 ◽  
pp. 107970
Author(s):  
Cássio Marinho Campelo ◽  
Igor Carvalho Pinheiro ◽  
Bruno de Melo Tavares ◽  
Guilherme Alves de Lima Henn ◽  
Camila Fernandes ◽  
...  
Keyword(s):  
Visceral Leishmaniasis ◽  
Complement Receptors ◽  
Type 3

scholarly journals Tipping the balance: intricate roles of the complement system in disease and therapy

2021 ◽  
Author(s):  
Richard B. Pouw ◽  
Daniel Ricklin
Keyword(s):  
Complement System ◽  
Host Cells ◽  
Great Promise ◽  
Effector Functions ◽  
Complement Inhibitors ◽  
Age Related ◽  
Recent Developments ◽  
The Complement System ◽  
Excessive Activation ◽  
Insight Into

AbstractThe ability of the complement system to rapidly and broadly react to microbial intruders, apoptotic cells and other threats by inducing forceful elimination responses is indispensable for its role as host defense and surveillance system. However, the danger sensing versatility of complement may come at a steep price for patients suffering from various immune, inflammatory, age-related, or biomaterial-induced conditions. Misguided recognition of cell debris or transplants, excessive activation by microbial or damaged host cells, autoimmune events, and dysregulation of the complement response may all induce effector functions that damage rather than protect host tissue. Although complement has long been associated with disease, the prevalence, impact and complexity of complement’s involvement in pathological processes is only now becoming fully recognized. While complement rarely constitutes the sole driver of disease, it acts as initiator, contributor, and/or exacerbator in numerous disorders. Identifying the factors that tip complement’s balance from protective to damaging effects in a particular disease continues to prove challenging. Fortunately, however, molecular insight into complement functions, improved disease models, and growing clinical experience has led to a greatly improved understanding of complement’s pathological side. The identification of novel complement-mediated indications and the clinical availability of the first therapeutic complement inhibitors has also sparked a renewed interest in developing complement-targeted drugs, which meanwhile led to new approvals and promising candidates in late-stage evaluation. More than a century after its description, complement now has truly reached the clinic and the recent developments hold great promise for diagnosis and therapy alike.

scholarly journals Biosynthetic homeostasis and resilience of the complement system in health and infectious disease

EBioMedicine ◽  
2019 ◽  
Vol 45 ◽  
pp. 303-313 ◽  
Author(s):  
Esther Willems ◽  
Wynand Alkema ◽  
Jenneke Keizer-Garritsen ◽  
Anouk Suppers ◽  
Michiel van der Flier ◽  
...  
Keyword(s):  
Infectious Disease ◽  
Complement System ◽  
The Complement System

scholarly journals Cellular Membrane Type-1 Matrix Metalloproteinase (MT1-MMP) Cleaves C3b, an Essential Component of the Complement System

2004 ◽  
Vol 279 (45) ◽  
pp. 46551-46557 ◽  
Author(s):  
Dmitri V. Rozanov ◽  
Alexei Y. Savinov ◽  
Vladislav S. Golubkov ◽  
Tatiana I. Postnova ◽  
Albert Remacle ◽  
...  
Keyword(s):  
Matrix Metalloproteinase ◽  
Complement System ◽  
Cellular Membrane ◽  
Essential Component ◽  
Membrane Type ◽  
The Complement System

Interference with the Complement System by Tumor Cell Membrane Type-1 Matrix Metalloproteinase Plays a Significant Role in Promoting Metastasis in Mice

2006 ◽  
Vol 66 (12) ◽  
pp. 6258-6263 ◽  
Author(s):  
Dmitri V. Rozanov ◽  
Alexei Y. Savinov ◽  
Vladislav S. Golubkov ◽  
Stephen Tomlinson ◽  
Alex Y. Strongin
Keyword(s):  
Cell Membrane ◽  
Matrix Metalloproteinase ◽  
Tumor Cell ◽  
Significant Role ◽  
Complement System ◽  
Tumor Cell Membrane ◽  
Membrane Type ◽  
The Complement System

scholarly journals OSTEOARTHRITIS AND IMMUNITY

2021 ◽  
Vol 29 (1) ◽  
pp. 44-51
Author(s):  
Irina Momcheva ◽  
I. Kazmin ◽  
S. Hristova ◽  
V. Madjova
Keyword(s):  
Complement System ◽  
Cell Membranes ◽  
Cartilage Damage ◽  
Joint Damage ◽  
Innate Immune ◽  
Low Grade ◽  
Complement Receptors ◽  
Molecular Patterns ◽  
Low Grade Inflammation ◽  
The Complement System

Abstract         Low-grade inflammation is part of the pathogenesis of osteoarthritis (OA) from its earliest stages and contributes to the acceleration of the degenerative process. Innate immunity has a leading role in it.        Activation of the innate immune response is initiated by stimulation of the receptors on the cell membrane to recognize the secreted PAMPs (pathogen-associated molecular patterns). However, PAMPs can also be activated by endogenous damage-related molecular patterns (DAMPs). The group of DAMPs also includes toll-like receptors (TLRs).The disruption of matrix homeostasis in the course of OA is an example of activation of these receptors in chronic damage.      The complement system is a key element of the innate immune system. It is one of the serum enzyme systems whose function is to opsonize antigens. The complement receptors on the surface of the cell membranes adhere to the targets for phagocytosis. The C3R fraction activates the complement cascade itself, as well as the oxygen metabolism of the cell, which is essential for the phagocytosis. The cartilage damage products released during joint damage are a separate class of potent complement modulators.     Complement fractions bind to complement receptors on the surface of the chondrocyte and the synoviocyte cell membranes by TLR. The complement system is involved in many processes in the course of osteoarthritis: chondrocyte degeneration, ECM degradation, low-grade inflammation in the osteoarthritis, cell lysis, unbalanced bone remodeling, osteophyte formation, and neoangiogenesis. Whether drug control of complement activation may be a future therapeutic strategy in the treatment of OA and prevent its progression is a subject of future studies.

scholarly journals Isolation of complement-fragment-iC3b-binding proteins by affinity chromatography. The identification of p150,95 as an iC3b-binding protein

1985 ◽  
Vol 231 (1) ◽  
pp. 233-236 ◽  
Author(s):  
K J Micklem ◽  
R B Sim
Keyword(s):  
Polymorphonuclear Leucocytes ◽  
Complement Receptors ◽  
Β Subunit ◽  
Homologous Proteins ◽  
Human Spleen ◽  
Bivalent Cations ◽  
Complement Component C3 ◽  
Additional Protein ◽  
Type 3

The proteins from labelled human spleen membranes and polymorphonuclear leucocytes which bind to the iC3b fragment of complement component C3 were prepared by iC3b-Sepharose chromatography in the presence of bivalent cations. Complement receptor type 3(CR3) was eluted from iC3b-Sepharose by removal of bivalent cations. Complement receptors type 1 and 2 (present in spleen but not in polymorphonuclear leucocytes) were sequentially eluted by an NaCl gradient. An additional protein of Mr 135 000 was eluted from iC3b-Sepharose under the same conditions as those used to elute CR3. Preabsorption of the starting material on an anti-(CR3 β-subunit) antibody column before iC3b-Sepharose chromatography removed the α- and β-chains of CR3 and the 135 000-Mr protein. Preabsorption with iC3b-Sepharose before the anti-(CR3 β-subunit) antibody column showed that iC3b binds CR3 and p150,95, the smallest member of the group of three homologous proteins that share the same β-subunit.

scholarly journals Complement Proteins as Soluble Pattern Recognition Receptors for Pathogenic Viruses

Viruses ◽  
2021 ◽  
Vol 13 (5) ◽  
pp. 824
Author(s):  
Valarmathy Murugaiah ◽  
Praveen M. Varghese ◽  
Nazar Beirag ◽  
Syreeta De Cordova ◽  
Robert B. Sim ◽  
...  
Keyword(s):  
Complement System ◽  
Membrane Attack Complex ◽  
Factor H ◽  
Complement Components ◽  
Diverse Range ◽  
Effector Functions ◽  
Pathogenic Viruses ◽  
Viral Survival ◽  
Chemotactic Factors ◽  
The Complement System

The complement system represents a crucial part of innate immunity. It contains a diverse range of soluble activators, membrane-bound receptors, and regulators. Its principal function is to eliminate pathogens via activation of three distinct pathways: classical, alternative, and lectin. In the case of viruses, the complement activation results in effector functions such as virion opsonisation by complement components, phagocytosis induction, virolysis by the membrane attack complex, and promotion of immune responses through anaphylatoxins and chemotactic factors. Recent studies have shown that the addition of individual complement components can neutralise viruses without requiring the activation of the complement cascade. While the complement-mediated effector functions can neutralise a diverse range of viruses, numerous viruses have evolved mechanisms to subvert complement recognition/activation by encoding several proteins that inhibit the complement system, contributing to viral survival and pathogenesis. This review focuses on these complement-dependent and -independent interactions of complement components (especially C1q, C4b-binding protein, properdin, factor H, Mannose-binding lectin, and Ficolins) with several viruses and their consequences.

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