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COMPLEMENT - Crossref

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Last Updated: 03 July 2022

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Increase in the Complement Activation Product C4d and the Terminal Complement Complex sC5b-9 Is Associated with Disease Severity and a Fatal Outcome in Necrotizing Soft-Tissue Infection

The complement system is a key during the adaptive immune response and may be a promising target to reduce the inflammatory response, potentially improving the clinical results. Patients were enrolled in NSTI and sampled blood at admission and then daily for the following three days, and then for the following three days. The Simplified Acute Physiology Score II's negative correlations between C4c and C3dg were negatively correlated with Simplified Acute Physiology Score II's simplified Acute Physiology Score II. Patients with septic shock had higher baseline TCC levels than those in non-shock patients. In multivariate Cox regression studies, elevated baseline C4d, and a mixture of high C4d and TCC were associated with elevated 30-day mortality. Both C4d and TCC were found to have a negative predictive value of 0. 87. In patients with NSTI, complement activation was linked to the severity of the disease, according to the study. C4d and TCC, as a result of elevated 30-day mortality, are associated with elevated 30-day mortality.

Source link: https://doi.org/10.1159/000520496


Complement Factor I Deficiency, a study on prevalence and impacts on complement dysregulation and health.

The complement system is made up of a complex proteolytic cascade of more than 50 soluble and membranous proteins, of which complement Factor I is a key protease that controls the cascade by activation of C3b and C4b and their downstream action in terminal membrane attack complex formation. Result : Bacterial infections are the most common inflammatory disease in FI deficient individuals. According to our report, symptoms often start early in childhood, with 80% of the cases reported in children under the age of 18 years old, indicating that FI deficiency is a pediatric disorder. Conclusions : We present the first comprehensive meta-analysis of FI-deficiency of 135 cases presented in the literature and have developed a new method to assess prospective therapeutic agents for their ability to treat FI deficiencies.

Source link: https://doi.org/10.21203/rs.3.rs-1598901/v1


Complement C3a and C3a Receptor Activation Mediates Podocyte Injuries in the Mechanism of Primary Membranous Nephropathy

This report looked at the role of C3a and the C3a receptor in MN pathogenesis. Methods and methods were evaluated for the C3aR expression in kidneys and blood C3a samples of MN patients. After exposure to MN plasma +/-u2212 C3aR blockade, human podocyte damage was assessed. On day 0 or after proteinuria, Heymann nephritis was administered to rats with Heymann nephritis. Human tubular cells exposed to MN plasma showed an elevated proliferation of PLA2R, C3aR, and Wnt3/u03b2 -catenin, decreased expression of synaptopodin and migration function, downregulated Bcl-2, and reduced cell viability, reduced cell viability, and reduced cell viability. C3aR's elevated plasma C3a levels and overexpression of C3aR were also reduced. IgG levels decreased, but not completely, with less deposition of rat IgG in glomeruli and subsequent decline of C1q, factor B, and C5b-9. Conclusion C3a anaphylatoxin is a key mediator of complement-mediated podocyte damage in Minnesota.

Source link: https://doi.org/10.1681/asn.2021101384


Inside-Out of Complement in Cancer

Although most studies link complement in cancer to complement activation in the extracellular space, the discovery of complement intracellular activation raises the question: what is the significance of this process for malignancy? We discuss complement's role in cancer here, including extra and intracellular pathways of complement activation and spatial distribution of complement proteins in tumors and periphery, as well as offering our take on complement as biomarker and target for cancer therapy.

Source link: https://doi.org/10.3389/fimmu.2022.931273


CD59: A long-known complement inhibitor has advanced to a blood group system

Abstract The blood group system number 35 is based on CD59, a 20-kDa membrane glycoprotein that is present on a large number of different cells, including erythrocytes, and erythrocytes. The main function of CD59 is to shield cells from complement attack. Other aspects of CD59's cellular immunity are less well defined. Patients with paroxysmal nocturnal hemoglobinuria have a varied proportion of red blood cell clones with a defect in GPI-anchored proteins, including CD59. Despite the fact that CD59 has been classified as a membrane protein for more than 25 years, an alloantibody directed against CD59 was discovered only recently. The International Society for Blood Transfusion Red Cell Immunogenetics and Blood Group Terminology Working Party recognized CD59 as a blood group system in 2014, the International Society for Blood Transfusion Red Cell Immunogenetics and Blood Group Terminology Working Party's Red Cell Immunogenetics and Blood Group Terminology Working Party's signature in 2014. Null alleles are the only three alleles known to date, with null alleles being the only three alleles known to date. The use of the complement inhibitor eculizumab in one published study resulted in a dramatic improvement of the clinical situation.

Source link: https://doi.org/10.21307/immunohematology-2019-083


Persistent complement-dependent anti-AnWj in a lymphoproliferative disorder: a case study and review

Abstract AnWj is a high-incidence antigen present on the red blood cells of over 99% of the general population. For stage IVa mantle cell lymphoma, a 58-year-old man underwent autologous hematopoietic stem cell transplantation. The graft AnWj's downregulation in this patient is unknown, and it is of utmost importance.

Source link: https://doi.org/10.21307/immunohematology-2019-179


Review: complement receptor 1 therapeutics for prevention of immune hemolysis

Abstract: The complement system plays a vital role in fighting viruses and is a key link between the innate and adaptive immune responses. Both intravascular and extravascular damage can result in vascular and extravascular damage in the transfusion medicine setting. Complement receptor 1 is a large single-pass glycoprotein that is expressed in a variety of cell types in blood, including RBCs and immune cells. In addition, it will be demonstrated in a live mouse model of transfusion reactions demonstrating that recombinant soluble forms of CR1 will reduce complement-mediated RBC destruction, prolonging the survival of transfused RBCs.

Source link: https://doi.org/10.21307/immunohematology-2019-402


Quantitation of red cell-bound immunoglobulins and complement in lymphoma patients

Quantitative ELISA may be useful in determining the amount of red blood cell-associated immunoglobulins in patients of autoimmune hemoglobulinemia. Autobiotic hemolysis is a component of anemia in patients with low-grade lymphomas. RBC-associated IgG and complement are an excellent tool for monitoring the effects of immune hemolysis therapy in patients with immune hemolysis.

Source link: https://doi.org/10.21307/immunohematology-2019-597

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions