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Distinct roles for the complement regulators factor H and Crry in protection of the kidney from injury.
Laskowski J, Renner B, Le Quintrec M, Panzer S, Hannan JP, Ljubanovic D, Ruseva MM, Borza DB, Antonioli AH, Pickering MC, Holers VM, Thurman JM
(2016) Kidney Int 90: 109-22
MeSH Terms: Animals, Complement C3, Complement Factor H, Complement Pathway, Alternative, Glomerulonephritis, Kidney Glomerulus, Male, Mice, Mice, Inbred C57BL, Mice, Knockout, Mutation, Receptors, Complement
Show Abstract · Added December 2, 2016
Mutations in the complement regulatory proteins are associated with several different diseases. Although these mutations cause dysregulated alternative pathway activation throughout the body, the kidneys are the most common site of injury. The susceptibility of the kidney to alternative pathway-mediated injury may be due to limited expression of complement regulatory proteins on several tissue surfaces within the kidney. To examine the roles of the complement regulatory proteins factor H and Crry in protecting distinct renal surfaces from alternative pathway mediated injury, we generated mice with targeted deletions of the genes for both proteins. Surprisingly, mice with combined genetic deletions of factor H and Crry developed significantly milder renal injury than mice deficient in only factor H. Deficiency of both factor H and Crry was associated with C3 deposition at multiple locations within the kidney, but glomerular C3 deposition was lower than that in factor H alone deficient mice. Thus, factor H and Crry are critical for regulating complement activation at distinct anatomic sites within the kidney. However, widespread activation of the alternative pathway reduces injury by depleting the pool of C3 available at any 1 location.
Copyright © 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.
1 Communities
1 Members
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12 MeSH Terms
Engineering complement activation on polypropylene sulfide vaccine nanoparticles.
Thomas SN, van der Vlies AJ, O'Neil CP, Reddy ST, Yu SS, Giorgio TD, Swartz MA, Hubbell JA
(2011) Biomaterials 32: 2194-203
MeSH Terms: Animals, Biocompatible Materials, Complement Activation, Complement C3, Complement Pathway, Alternative, Materials Testing, Mice, Mice, Inbred C57BL, Nanoparticles, Polypropylenes, Sulfides, Surface Plasmon Resonance, Surface Properties, Vaccines
Show Abstract · Added March 20, 2014
The complement system is an important regulator of both adaptive and innate immunity, implicating complement as a potential target for immunotherapeutics. We have recently presented lymph node-targeting, complement-activating nanoparticles (NPs) as a vaccine platform. Here we explore modulation of surface chemistry as a means to control complement deposition, in active or inactive forms, on polypropylene sulfide core, block copolymer Pluronic corona NPs. We found that nucleophile-containing NP surfaces activated complement and became functionalized in situ with C3 upon serum exposure via the alternative pathway. Carboxylated NPs displayed a higher degree of C3b deposition and retention relative to hydroxylated NPs, upon which deposited C3b was more substantially inactivated to iC3b. This in situ functionalization correlated with in vivo antigen-specific immune responses, including antibody production as well as T cell proliferation and IFN-γ cytokine production upon antigen restimulation. Interestingly, inactivation of C3b to iC3b on the NP surface did not correlate with NP affinity to factor H, a cofactor for protease factor I that degrades C3b into iC3b, indicating that control of complement protein C3 stability depends on architectural details in addition to factor H affinity. These data show that design of NP surface chemistry can be used to control biomaterials-associated complement activation for immunotherapeutic materials.
Copyright © 2010 Elsevier Ltd. All rights reserved.
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1 Members
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14 MeSH Terms
The effect on patient health of using reprocessed artificial kidneys.
Lowrie EG, Hakim RM
(1980) Proc Clin Dial Transplant Forum 10: 86-91
MeSH Terms: Adolescent, Adult, Antibody Formation, Blood Coagulation, Blood Flow Velocity, Blood Urea Nitrogen, Complement Pathway, Alternative, Creatinine, Humans, Isoantibodies, Kidney Failure, Chronic, Kidneys, Artificial, Leukopenia, Long-Term Care, MNSs Blood-Group System
Added May 20, 2014
0 Communities
1 Members
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15 MeSH Terms
Increased expression of the C3b receptor by neutrophils and complement activation during haemodialysis.
Lee J, Hakim RM, Fearon DT
(1984) Clin Exp Immunol 56: 205-14
MeSH Terms: Biocompatible Materials, Cells, Cultured, Complement Activation, Complement C5, Complement C5a, Complement Pathway, Alternative, Humans, Leukocyte Count, Membranes, Artificial, Neutrophils, Receptors, Complement, Receptors, Complement 3b, Renal Dialysis, Time Factors
Show Abstract · Added May 20, 2014
Activation of complement and the relative number of C3b receptors expressed by neutrophils was assessed in patients undergoing haemodialysis with new and reused cellulosic membranes, and with polymethylmethacrylate (PMMA) membranes. Activation of complement was assessed by radioimmunoassay of plasma C3adesArg, and neutrophil C3b receptors were measured by fluorescent flow cytometry of cells indirectly stained with F(ab')2 anti-C3b receptor. During first use of cellulosic dialysis membranes by four patients, the mean expression of C3b receptors by neutrophils in blood taken from the afferent line of the extra-corporeal system after 10, 20, 60 and 120 min of dialysis increased to 127, 189, 255 and 296%, respectively. The mean plasma C3adesArg concentrations in the corresponding samples of blood were 225, 320, 236 and 160% of the pre-dialysis levels. During third and fifth use of the same membranes by these patients, the mean C3b receptor expression by neutrophils did not exceed 150% of the predialysis determination, and correspondingly minimal increases in plasma C3adesArg were observed. Analysis of blood taken simultaneously from the afferent and efferent lines of the first use cellulosic dialysis system indicated that the increase in C3b receptor expression by neutrophils and generation of C3adesArg occurred when blood came in contact with the dialysis membrane. Haemodialysis of four additional patients with the non-complement activating PMMA membrane caused only modest or no increases in neutrophil C3b receptors. Thus, complement activation in vivo is associated with up-regulation of neutrophilic C3b receptors, indicating that this cellular response previously described only in model, in vitro systems, is a physiological mechanism by which this cell can augment its capacity for responding to C3b opsonized material.
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1 Members
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14 MeSH Terms