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A Monoclonal Antibody That Provides a Model for C3 Nephritic Factors.
Monoclon Antib Immunodiagn Immunother
February 2023
Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, USA.
Complement is a major innate defense system that protects the intravascular space from microbial invasion. Complement activation results in the assembly of C3 convertases, serine proteases that cleave complement protein C3, generating bioactive fragments C3a and C3b. The complement response is rapid and robust, largely due to a positive feedback regulatory loop mediated by alternative pathway (AP) C3 convertase.
View Article and Find Full Text PDFRole of Complement Properdin in Renal Ischemia-Reperfusion Injury.
Curr Gene Ther
April 2019
Department of Infection, Immunity and Inflammation, College of Life Sciences, University of Leicester, Leicester, United Kingdom.
Renal Ischemia-Reperfusion Injury (IRI) is one of the main causes of Acute Kidney Injury (AKI), and may lead to chronic kidney disease. The high mortality rate of AKI has not changed in the last 5 decades due to non-recognition, nephrotoxin exposure, delayed diagnosis and lack of specific intervention. Complement activation plays important roles in IRI-induced AKI because of its association with immunity, inflammation, cell death and tissue repair.
View Article and Find Full Text PDFQuantitative Modeling of the Alternative Pathway of the Complement System.
PLoS One
August 2016
Department of Bioengineering, University of California Riverside, Riverside, California, United States of America.
The complement system is an integral part of innate immunity that detects and eliminates invading pathogens through a cascade of reactions. The destructive effects of the complement activation on host cells are inhibited through versatile regulators that are present in plasma and bound to membranes. Impairment in the capacity of these regulators to function in the proper manner results in autoimmune diseases.
View Article and Find Full Text PDFQuantitative analysis of factor P (Properdin) in monkey serum using immunoaffinity capturing in combination with LC-MS/MS.
Bioanalysis
December 2016
Department of Drug Metabolism & Pharmacokinetics, Novartis Institutes for BioMedical Research, East Hanover, NJ 07936, USA.
Aim: Factor P (Properdin), an endogenous glycoprotein, plays a key role in innate immune defense. Its quantification is important for understanding the pharmacodynamics (PD) of drug candidate(s).
Results: In the present work, an immunoaffinity capturing LC-MS/MS method has been developed and validated for the first time for the quantification of factor P in monkey serum with a dynamic range of 125 to 25,000 ng/ml using the calibration standards and QCs prepared in factor P depleted monkey serum.
Combination of factor H mutation and properdin deficiency causes severe C3 glomerulonephritis.
J Am Soc Nephrol
January 2013
Department of Pharmacology and Institute for Translational Medicine and Therapeutics, University of Pennsylvania, Perelman School of Medicine, Philadelphia, PA 19104, USA.
Factor H (fH) and properdin both modulate complement; however, fH inhibits activation, and properdin promotes activation of the alternative pathway of complement. Mutations in fH associate with several human kidney diseases, but whether inhibiting properdin would be beneficial in these diseases is unknown. Here, we found that either genetic or pharmacological blockade of properdin, which we expected to be therapeutic, converted the mild C3 GN of an fH-mutant mouse to a lethal C3 GN with features of human dense deposit disease.
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