Relevant bibliographies by topics / C3b

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  2. Dissertations / Theses
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Academic literature on the topic 'C3b'

Author: Grafiati
Published: 4 June 2021
Last updated: 10 March 2023

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Journal articles on the topic "C3b"

1

Quigg, R. J., J. J. Alexander, C. F. Lo, A. Lim, C. He, and V. M. Holers. "Characterization of C3-binding proteins on mouse neutrophils and platelets." Journal of Immunology 159, no. 5 (September 1, 1997): 2438–44. http://dx.doi.org/10.4049/jimmunol.159.5.2438.

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Abstract In the mouse, MCR1 and MCR2 on B lymphocytes are encoded by alternatively spliced Cr2 gene transcripts. Immune adherence receptors that bind C3 are present on mouse platelets and unstimulated neutrophils, yet they are not MCR1 or MCR2. To examine C3b- and C3d-binding proteins on mouse platelets and neutrophils, we performed C3b and C3d affinity chromatography as well as immunoprecipitation studies using previously described Ab to MCR1/MCR2 (mAb clones 8C12, 7G6, and 7E9 and polyclonal Ab BRN-1). Mouse neutrophils contained a 190-kDa membrane protein that specifically bound to C3b-Sepharose. Preabsorption of neutrophil proteins with anti-MCR1/MCR2 Ab did not affect the recovery of the 190-kDa C3b-binding protein by subsequent C3b affinity chromatography. Thus, this protein is immunologically distinct from the previously described MCR1 and MCR2 proteins. By virtue of its size and C3b-binding capacity, the 190-kDa protein was named C3bR-190. C3bR-190 was also apparent on platelets, but in reduced amounts. BRN-1 anti-MCR1/MCR2 Ab immunoprecipitated proteins of 125 and 150 kDa from surface-radiolabeled mouse platelets, which specifically bound to C3d-Sepharose. However, these proteins were not identified by mAb to MCR2, thus distinguishing them from previously described MCR2. These proteins were named C3dR-125 and C3dR-150. Therefore, we have identified a 190-kDa C3b-binding protein on mouse neutrophils and 125- and 150-kDa C3d-binding proteins on mouse platelets. These appear to be distinct from the heretofore identified mouse B lymphocyte MCR1 and MCR2. The identity of these C3b- and C3d-binding proteins on mouse neutrophils and platelets awaits further study.
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Sahu, A., B. K. Kay, and J. D. Lambris. "Inhibition of human complement by a C3-binding peptide isolated from a phage-displayed random peptide library." Journal of Immunology 157, no. 2 (July 15, 1996): 884–91. http://dx.doi.org/10.4049/jimmunol.157.2.884.

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Abstract We have screened a phage-displayed random peptide library for binding to C3b, the proteolytically activated form of complement component C3, and have identified a novel peptide that suppresses complement activation. This phage-displayed peptide bound to C3, C3b, and C3c, but not to C3d, indicating that it binds to the C3c region of C3. A synthetic 27-amino acid peptide corresponding to the phage-displayed peptide also bound to C3 and C3 fragments and inhibited both the classical and alternative pathways of complement activation. The inhibition of complement activation was reversible. Studies with overlapping peptides indicated that the functional activity was located in the cyclic 13-amino acid N-terminal region (ICVVQDWGHHRCT) of the parent peptide. Reduction and alkylation of this 13-residue synthetic peptide destroyed its inhibitory activity. Analysis of the mechanism of inhibition revealed that the peptide inhibited C3 cleavage in normal human serum as well as when the alternative pathway was reconstituted with purified complement components, and the observed inhibition was not due to sterically hindered access to the C3a/C3b cleavage site. Further, the peptide did not inhibit the cleavage of factor B, indicating that it did not affect the interaction of CA with factor B or the formation of C3b,Bb. The peptide also had no effect on the binding of properdin to C3, demonstrating that the observed inhibition of C3 cleavage in normal human serum was not due in part to its effect on the properdin-stabilized C3 convertase, C3b,Bb,P. These results indicate that the peptide we have identified interacts with C3 to inhibit its activation.
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Farries, T. C., P. J. Lachmann, and R. A. Harrison. "Analysis of the interactions between properdin, the third component of complement (C3), and its physiological activation products." Biochemical Journal 252, no. 1 (May 15, 1988): 47–54. http://dx.doi.org/10.1042/bj2520047.

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The interactions of properdin with both surface-bound and fluid-phase C3 (the third component of complement) and its activation products have been investigated by using a purified preparation of the ‘native’ form. At physiological ionic strength, a weak interaction with cell-bound C3b (the larger activation fragment of C3) could be demonstrated. In the presence of Factor B this interaction was enhanced, and further enhancement was seen when C3bBb sites were formed on the erythrocytes. The avidities of properdin for cell-bound iC3b (the initial product of Factors I and H action on C3b) and C3b were compared at low ionic strength, with that measured for iC3b being less than that for C3b. In contrast, the affinities of properdin for fluid-phase C3b, iC3b and C3c (the larger product of Factors I and H or CR1 (the C3b receptor) action on iC3b) were all very similar, and apparently much weaker than that for cell-bound C3b. No interaction with either native C3 or, more surprisingly, C3i (haemolytically inactive C3) could be detected. Properdin also inhibited Factor I binding to, and action upon, cell-bound C3b, but did not inhibit Factor I action on fluid-phase C3b. These data permit a more detailed description of the roles of properdin in the alternative pathway of complement activation, emphasizing its importance in concentrating activation at the activating surface.
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Fries, L. F., G. M. Prince, T. A. Gaither, and M. M. Frank. "Factor I co-factor activity of CR1 overcomes the protective effect of IgG on covalently bound C3b residues." Journal of Immunology 135, no. 4 (October 1, 1985): 2673–79. http://dx.doi.org/10.4049/jimmunol.135.4.2673.

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Abstract We have shown previously that C3b resides in a protected site when it is covalently bound to IgG (C3b-IgG). Such C3b displays a reduced affinity for factor H, with consequent enhanced survival in the presence of factors H and I and increased capacity for promoting alternative pathway consumption of C3. Because erythrocyte CR1 may be a major co-factor for factor I-mediated inactivation of immune complex-borne C3b in blood, we have examined the effect of covalently bound IgG on the C3b-CR1 interaction. Binding of monomeric C3b and C3b-IgG to human erythrocyte CR1 demonstrates identical ionic strength dependence for both species. Identical numbers of binding sites with indistinguishable affinities are detected by both ligands. Cleavage of the alpha'-chain of C3b and the alpha'-heavy chain of C3b-IgG proceeds at the same rate when erythrocyte CR1 serves as co-factor for factor I. Unlike factor H, CR1 supports a second cleavage of fluid-phase iC3b alpha'1 chain (free or bound to IgG) that generates C3c and a 33,000 m.w. fragment, which bears antigenic markers characteristic of C3g. Inactivation of C3b and C3b-IgG by CR1 and factor I also occurs at physiologic ionic strength, but proceeds very slowly relative to rates attainable with sub-physiologic inputs of factor H. CR1 does not recognize IgG-bound C3b as being in a protected site but, because of low binding affinity at physiologic ionic strength, is probably highly dependent on multivalent ligand-receptor interactions to efficiently exert its co-factor functions. Thus, inactivation of C3b-IgG heterodimers or small immune complexes bearing limited numbers of C3b residues may remain largely factor H-dependent in vivo, with resultant enhanced C3b survival.
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Tamerius, J. D., M. K. Pangburn, and H. J. Müller-Eberhard. "Detection of a neoantigen on human C3bi and C3d by monoclonal antibody." Journal of Immunology 135, no. 3 (September 1, 1985): 2015–19. http://dx.doi.org/10.4049/jimmunol.135.3.2015.

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Abstract A neoantigen was detected on human C3bi and C3d by using the monoclonal antibody (MoAb) 130. The antibody bound to EC3bi and EC3d cells but not to EC3b. Although highly purified C3bi or C3d strongly inhibited the binding of the antibody to EC3d, highly purified C3c had no such effect. Native C3, C3b, or C3(H2O) inhibited this binding only weakly. The neoantigen was also detected in serum after activation with zymosan or heat-aggregated IgG, and it was found bound to the aggregated IgG and zymosan particles. Plasma samples from patients with immunologic disorders were tested for this neoantigen, and 25 out of 43 samples tested were found to have levels of neoantigen corresponding to 2 to 11.5% complement activation, whereas 13 out of 14 normal donor plasmas contained amounts of neoantigen indicating much less than 1% complement activation.
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Kostavasili, I., A. Sahu, H. M. Friedman, R. J. Eisenberg, G. H. Cohen, and J. D. Lambris. "Mechanism of complement inactivation by glycoprotein C of herpes simplex virus." Journal of Immunology 158, no. 4 (February 15, 1997): 1763–71. http://dx.doi.org/10.4049/jimmunol.158.4.1763.

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Abstract Glycoprotein C (gC) of both herpes simplex virus type 1 (HSV-1) and HSV-2 interacts with complement C3b and protects the virus from complement-mediated neutralization. To study the mechanism by which gC modulates complement activation, we expressed both gC-1 and gC-2 in a baculovirus expression system. Baculovirus recombinants containing gC genes spanning the entire gC-1 sequence (gC-1-TMR) or only the extracellular domain(s) of gC-1, gC-2, or a deletion mutant of gC-1 lacking residues 33 through 123 were expressed in sf9 insect cells. Binding of the expressed proteins to human C3 and C3 fragments was assessed by direct and competition ELISA. All four expressed proteins bound to C3, C3b, and C3c but not to C3d, suggesting 1) that the binding sites for these proteins are located in the C3c region of C3; and 2) that gC, in contrast to other C3-binding proteins, interacts with native C3. We have also examined the interaction of native C3 with gC-1 expressed on the HSV-1-infected cells. Analogous to recombinant proteins, gC-1 expressed on the infected cells also bound to native C3. The ability of baculovirus-expressed gCs to inhibit the interaction of C3b with its ligands was also analyzed. We found that gC-1, but not gC-2, inhibited the binding of C5 and properdin to C3b and also inhibited the alternative pathway-mediated lysis of rabbit erythrocytes. Inhibition of alternative pathway-mediated lysis and properdin binding to C3b, but not of C5 binding to C3b, required the transmembrane segment of the gC-1. The specificity of gC interactions was examined by studying the interaction of gC with C3 from various species. In contrast to properdin, both gCs bound to cobra C3; this finding suggests that gC-1 and properdin bind to different sites on C3b. Further analyses suggested that gC-1 sterically hindered access of C5 and properdin to C3b.
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Villiers, Marie-Bernadette, Christian L. Villiers, Anne-Marie Laharie, and Patrice N. Marche. "Amplification of the Antibody Response by C3b Complexed to Antigen Through an Ester Link." Journal of Immunology 162, no. 6 (March 15, 1999): 3647–52. http://dx.doi.org/10.4049/jimmunol.162.6.3647.

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Abstract Complement C3 has been described as playing an important role in the cell-mediated immune response. C3b has the capacity to covalently bind Ag and then to stimulate in vitro Ag presentation to T lymphocytes. To verify this observation in vivo, we prepared and purified covalent human C3b-Ag complexes using lysozyme (HEL) as Ag. The characterization of these HEL-C3b complexes indicates that they are representative of those susceptible to be generated in physiological conditions. Mice were immunized with 0.1 to 0.6 μg of either free HEL, HEL + C3b, HEL-C3b, or HEL + CFA. Response was assessed after two i.p. injections by quantification of specific Ab production. Immunization with either HEL-C3b complexes or HEL + CFA leads to anti-HEL IgG production whereas free HEL or HEL + C3b was ineffective. Either HEL-C3b or HEL + CFA immunizations led to a similar Ig subclasse patterns, including IgG1, IgG2a, IgA, and IgM. Our experiments provide the first evidence for modulation of specific Ab response by C3b when it is bound to Ag through a physiological-like link. Taken together with previous data concerning Ab response following recombinant HEL-C3d immunization, cellular events such as processing of C3b-Ag by APC and recognition by T lymphocytes, this present result underlines the importance of C3b and its fragments in stimulation of the immune system, through the multiplicity and complementarity of its interactions.
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Sahu, Arvind, Stuart N. Isaacs, Athena M. Soulika, and John D. Lambris. "Interaction of Vaccinia Virus Complement Control Protein with Human Complement Proteins: Factor I-Mediated Degradation of C3b to iC3b1 Inactivates the Alternative Complement Pathway." Journal of Immunology 160, no. 11 (June 1, 1998): 5596–604. http://dx.doi.org/10.4049/jimmunol.160.11.5596.

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Abstract Vaccinia virus complement control protein (VCP) is a virulence determinant of vaccinia virus that helps protect the virus from the complement attack of the host. To characterize the interaction of VCP with C3 and C4 and understand the mechanism by which VCP inactivates complement, we have expressed VCP in a yeast expression system and compared the biologic activity of the purified protein to that of human factor H and complement receptor 1 (CR1). Recombinant VCP bound to C3 and the proteolytically cleaved form of C3 (C3b), but not to the 135,300-m.w. fragment of C3 generated using elastase (C3c) and the 35,000-m.w. fragment of C3 generated using elastase (C3d) and inhibited both the classical and alternative pathways of complement activation. Although rVCP was less effective at inhibiting the alternative pathway than factor H or CR1, it was more effective than factor H at inhibiting the classical pathway. Unlike factor H, rVCP was unable discriminate between alternative pathway-mediated lysis of rabbit and sheep E. A comparison of the cofactor activity in factor I-mediated cleavage of C3b suggested that in contrast to factor H and CR1, which displayed cofactor activity for the three sites, rVCP displayed cofactor activity primarily for the first site, leading to generation of C3b cleaved by factor I between Arg1281-Ser1282 (iC3b1). Its cofactor activity for C4b cleavages was similar to that of soluble complement receptor type 1. Purification and functional analysis of iC3b1 showed that it was unable to interact with factor B to form the alternative pathway C3 convertase, C3b,Bb. These results suggest that the interaction of VCP with C3 is different from that of factor H and CR1 and that VCP-supported first cleavage of C3b by factor I is sufficient to render C3b nonfunctional.
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Risitano, Antonio M., Caterina Pascariello, Luigi Del Vecchio, Christopher J. Horvath, Masha Fridkis-Hareli, V. Michael Holers, Margaret A. Lindorfer, and Ronald P. Taylor. "C3-Mediated Extravascular Hemolysis In Paroxysmal Nocturnal Hemoglobinuria: An In Vitro Model to Dissect Complement C3 Activation Comparing the Effects of Complement Inhibitors Eculizumab, 3E7 and TT30 on C3 Fragment Processing and Hemolysis of PNH Erythrocytes." Blood 116, no. 21 (November 19, 2010): 637. http://dx.doi.org/10.1182/blood.v116.21.637.637.

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Abstract Abstract 637 PNH is characterized by complement (C)-mediated chronic intravascular hemolysis (IVH) due to the absence of CD55 and CD59 on erythrocytes (E) and subsequent impaired C regulation. C alternative pathway (CAP)-derived normal ongoing low level activity (termed the tickover mechanism) is the pivotal initial step, which subsequently leads to C3 fragment (C3frag) deposition on E followed by membrane attack complex (MAC)-mediated IVH. C3frag processing on E proceeds from the initially covalently attached C3b form that is serially converted through proteolysis, mediated on E by factor I and cofactors factor H and complement receptor 1 (CR1), to iC3b and then to C3d as forms that all remain membrane-bound. To develop an improved mechanistic understanding of this process in PNH, which results in C3frag accumulation and extravascular hemolysis (EVH) in vivo during eculizumab (Ecu) treatment, herein we exploited an in vitro model to characterize and dissect C3frag generation after CAP activation on PNH E. We used monoclonal antibodies (mAbs) specific for the different C3 fragments, including C3b/iC3b (mAbs 2C5, 3C11, 3E7, 7C12 and 8E11) and C3b/iC3b/C3d (mAbs A702, 1H8 and 14A10). We also investigated the effect of the C inhibitors (C-Inh) Ecu, 3E7 (a CAP-inhibitory anti-C3b/iC3b mAb) and TT30 (a cell surface-targeted CAP-inhibitory complement receptor 2/factor H fusion protein) on C3frag accumulation and hemolysis of PNH E. E from PNH patients, either naïve or on Ecu treatment, were washed and incubated in ABO-matched acidified normal human serum (aNHS). Assessment of hemolysis and C3 activation and processing was performed by serial flow cytometry analyses of both intact E and E ghosts, as previously described (Risitano et al, Blood 2009; Lindorfer et al, Blood 2010). We first studied E from PNH patients on Ecu, which were known to be C3frag+ using an anti-C3 polyclonal Ab (pAb). Only the anti-C3b/iC3b/C3d mAbs A702, 1H8 and 14A10 demonstrated binding to these PNH E, with a pattern overlapping with that of the anti-C3 pAb, while the anti-C3b/iC3b mAbs 2C5, 3C11, 3E7, 7C12 and 8E11 did not bind. To investigate the kinetics of generation of specific C3frag on PNH E, fresh E from untreated PNH patients that did not show either membrane-bound C3b/iC3b or C3d were exposed in vitro to aNHSs. Analysis at 1h and 24h revealed that intact E, which remained C3frag-negative, progressively decreased and finally disappeared, being transformed into C3b/iC3b+ and C3d+ ghosts. In the presence of Ecu (using serum from patients on Ecu treatment, drawn within 1h of dosing), the same experiments revealed a dramatic reduction of hemolysis, but residual CAP-mediated hemolysis in a process of pharmacodynamic breakthrough was confirmed by the presence of C3b/iC3b+, C3d+, CD59− E ghosts. More interestingly, intact E showed substantial C3frag deposition which progressed over time, initially characterized by the presence of C3b/iC3b and C3d, and subsequently converting after 24h exclusively into C3d+ E, with an identical phenotype as found in C3frag+ PNH E obtained from patients on Ecu. This result demonstrates that PNH E, despite exhibiting only C3d when recovered from patients, pass through an earlier phase where C3b/iC3b frag are present that can interact with their cognate receptors on fixed cells in liver and spleen during EVH in vivo. Both 3E7 and TT30 completely inhibited hemolysis, with an IC50 of 120 μg/mL for 3E7 and 30 μg/mL for TT30; consistent with their mechanism of action, both 3E7 and TT30 bound to PNH RBCs. No C3b/iC3b nor C3d was detected on surviving PNH E at any time, indicating that 3E7 and TT30 effectively inhibit the earliest phases of CAP activation involved in EVH. Similar results were obtained when E from PNH patients on Ecu were challenged in vitro with aNHS in the presence or absence of C-Inh. In conclusion, we demonstrate that CAP-mediated C3b/iC3b fixation to PNH RBCs is the early event leading to IVH or, in presence of Ecu, to C3frag deposition and subsequent EVH in vivo. Unlike Ecu, use of 3E7 or TT30 resulted in complete inhibition of hemolysis as well as CAP-mediated C3 activation, preventing C3b/iC3b and C3d deposition on intact PNH E. Thus, use of this model will allow assessment of the roles of both endogenous and therapeutic C regulators in CAP activation and C3 processing (and subsequent EVH) in PNH. Preclinical data suggest that TT30 is an optimal candidate agent to assess in vivo the effect of CAP inhibition in PNH patients. Disclosures: Risitano: Taligen Therapeutics: Consultancy, Research Funding. Horvath:Taligen Therapeutics: Employment. Fridkis-Hareli:Taligen Therapeutics: Employment. Holers:Taligen Therapeutics: Employment, Equity Ownership, Membership on an entity's Board of Directors or advisory committees, Patents & Royalties.
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Kaidoh, T., and I. Gigli. "Phylogeny of C4b-C3b cleaving activity: similar fragmentation patterns of human C4b and C3b produced by lower animals." Journal of Immunology 139, no. 1 (July 1, 1987): 194–201. http://dx.doi.org/10.4049/jimmunol.139.1.194.

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Abstract Functional and structural studies of the activated proteins of the complement system C4b and C3b have led to the identification of cleavage products resulting from the effect of the regulatory proteins, factor I, H, and C4b binding protein (bp). In this paper we report the results of studies that investigated the capacity of plasma or serum from a wide range of phylogenetic species to yield similar cleavage products. Sera and plasma from mammals, reptiles, amphibia, and fishes are capable of cleaving fluid phase human C4b and C3b, generating apparently the same fragments as observed using normal human serum: alpha 2, alpha 3, alpha 4 from the alpha' chain of C4b: and alpha-68, alpha-46, alpha-43, and alpha-30 from the alpha' chain of C3b. When C3b bound to a cell membrane is used C3c and C3dg are generated. The generation of these fragments from C3bi is a dose-dependent reaction. There is no correlation between the evolution of the species and the quantitative capability to degrade the substrates. Birds possess only a limited capability to degrade the alpha' chain of C4b and have no cleaving activity for C3b, whereas sera from more primitive vertebrate species (chondrichthyes and agnatha) fail to participate in the reaction. Contrary to other species, the proteins in fish serum or plasma responsible for the degradation of C4b and C3b show a unique requirement for Ca2+ ions. Magnesium and barium are less effective, and in their presence a 65,000 dalton intermediate product is observed. These results demonstrate that protein(s) displaying proteolytic activity for products of complement activation, probably related to I, H, and C4bp, are present in plasma of species whose evolution have preceded humans by 300 million years. Moreover, the recognition of human substrates and the generation of fragments identical to those produced by human serum suggests that human C4b and C3b share structural characteristics with their evolutionary ancestors in the serum or plasma of the species studied.
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Dissertations / Theses on the topic "C3b"

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Paramaswara, Bamini. "Characterization of the promoter for the human factor I (C3b/C4b inactivator) gene." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ34077.pdf.

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Jakob, Stephan Mathias. "Klinische und biochemische Aspekte des vollständigen, hereditären Komplement Faktor I-(C3b/C4b-Inaktivor)Mangels /." Bern, 1990. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.

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Holme, E. R. "C3b receptors (CR1) on peripheral human blood cells." Thesis, University of Glasgow, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.381473.

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Kucukkilic, Ezgi. "Copy number variation and relevance to disease of the complement C3b/C4b receptor 1 (CR1) gene." Thesis, University of Leicester, 2017. http://hdl.handle.net/2381/40701.

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The complement 3b/4b receptor 1 (CR1) gene is located at chromosome 1q32.2 in a cluster of complement-related genes. CR1 regulates both classical and alternative pathways of the complement system. CR1 is a major receptor for Plasmodium falciparum, and variation within the gene has been associated with different malarial clinical phenotypes. CR1 shows intragenic copy number variation (CNV) resulting in variation in protein length and number of C3b/C4b binding domains. Previously, CR1 was related to Alzheimer’s disease (AD) via complement system regulation. Furthermore, CR1 variation is responsible for the alleles of the Knops blood group, including McCoy and Swain-Langley. In this thesis, Novel paralogue ratio test (PRT) assays were developed to robustly type CNV of the low-copy repeat (LCR) regions (which defines the common CR1-A and CR1-B alleles, but also rarer alleles) within the gene in large cohorts, and an allele-specific hybridisation assay to genotype alleles of the Knops blood group system. Variation was analysed across global populations, and in the Tori-Bossito cohort (563 infants) from Benin, followed since birth to observe malaria acquisition and treatment. This showed that the Swain-Langley Sl2 polymorphism is not in strong linkage disequilibrium (LD) with the CNV, nor with other Knops blood group alleles. It appears to provide protection against early acquisition of malaria and subsequent number of malarial infections in the Tori-Bossito cohort but these results were not confirmed in an independent cohort (n=276). The association between the CR1-B allele and AD (early-onset (EOAD) and late-onset (LOAD)) was explored, showing that the CR1 risk loci (rs3818361, rs6656401 (only for EOAD) and rs6701713) were in moderate LD with CR1-B, but revealing no association between CR1-B (p=0.755) and EOAD (n=633). However, the CR1-B allele (risk) appears to be associated with LOAD (n=2185) with (p=0.015) and without (p=0.048) use of a junction fragment PCR assay.
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Birmingham, Daniel J. "The characterization of the baboon erythrocyte C3b binding protein /." The Ohio State University, 1989. http://rave.ohiolink.edu/etdc/view?acc_num=osu148767311411266.

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Chaumonnot, Killian. "La protéine de choc thermique Gp96 dans les macrophages au cours du stress du RE : Interaction avec le complément C3." Thesis, Bourgogne Franche-Comté, 2020. http://www.theses.fr/2020UBFCJ002.

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La protéine de stress Gp96, est une protéine du réticulum endoplasmique (RE) de la famille des HSP90, exprimée dans toutes les cellules. En situation de stress du RE, elle est induite et peut alors être exprimée au niveau membranaire et extracellulaire. Gp96 est connue pour moduler de manière ambivalente les réponses immunitaires, ayant des effets à la fois pro- et anti-inflammatoires. Bien qu’elle ait été montrée nécessaire pour la tolérance au microbiote des macrophages intestinaux, son rôle n’a pas été pas élucidé au niveau moléculaire. De plus, ses effets dans les macrophages en situation de stress du RE n’est pas connu, malgré leur implication dans de nombreuses pathologies. Dans ces travaux, nous montrons dans un premier temps que Gp96 est exprimée à la membrane des macrophages M2 et non des macrophages M1 dérivés de monocytes du sang périphérique de volontaires sains. Nous mettons en évidence que le stress du RE, généré par la perturbation de l’homéostasie calcique induite par la thapsigargine (Tg), a pour conséquence un switch du phénotype M2 vers un profil pro-inflammatoire dépendant de Gp96 fonctionnelle. Ce switch est associé à la diminution de l’expression membranaire de Gp96 et à sa sécrétion. Dans un second temps, nous démontrons que Gp96 interagit avec le complément C3 intracellulaire dans les macrophages M1 et M2. Cette interaction est plus importante dans les macrophages M2 stressés comparé aux M2 non stressés et, C3b, le fragment issu du clivage de C3, est présent uniquement dans le surnageant de culture des M2 stressés, et a pu de plus être co-immunoprécipité avec Gp96. Enfin, comme Gp96, le fragment inactivé de C3b, iC3b, est détecté uniquement à la membrane des M2 non stressés et sa présence dépend de Gp96 fonctionnelle. Ces résultats suggèrent que Gp96 membranaire et iC3b pourraient être des marqueurs des macrophages M2 anti-inflammatoires. Ils montrent que Gp96 est impliquée dans la modulation du phénotype M2 vers un profil pro-inflammatoire induite par une perturbation de l’homéostasie du calcium. Cet effet pourrait être lié à sa capacité à interagir avec le complément C3 dont les fragments de clivage C3a et C3b ont des effets pro-inflammatoires
The stress protein Gp96, is an endoplasmic reticulum (ER) protein of the HSP90 family, expressed in all cells. Under ER stress, it is induced and can then be expressed at the membrane and extracellular levels. Gp96 is known to have a dual role in immune responses, having both pro- and anti-inflammatory effects. Although it has been shown to be necessary for the tolerance of intestinal macrophages to the microbiota, its role has not been elucidated at the molecular level. Moreover, its effects in macrophages under ER stress are not known, despite their involvement in many pathologies. In this work, we first show that Gp96 is expressed at the membrane of M2 and not M1 macrophages derived from blood monocytes of healthy volunteers. We show that ER stress, generated by the disruption of calcium homeostasis induced by thapsigargine (Tg), results in a switch from the M2 phenotype to a functional Gp96-dependent pro-inflammatory profile. This switch is associated with the decrease in membrane expression of Gp96 and its secretion. In a second step, we demonstrate that Gp96 interacts with intracellular complement C3 in macrophages M1 and M2. This interaction is more important in stressed M2 macrophages than in untreated M2 and, C3b, the fragment resulting from the cleavage of C3, is present only in the culture supernatant of the stressed M2, and could moreover be co-immunoprecipitated with Gp96. Finally, like Gp96, the inactivated fragment of C3b, iC3b, is detected only at the membrane of unstressed M2 and its presence is dependent on functional Gp96. These results suggest that membrane Gp96 and iC3b could be markers of anti-inflammatory M2 macrophages. They show that Gp96 is involved in the modulation of the M2 phenotype towards a pro-inflammatory profile induced by a disruption of calcium homeostasis. This effect could be related to its ability to interact with the C3 complement whose C3a and C3b cleavage fragments have pro-inflammatory effects
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Ng, Y. C. "Complement and the C3b receptor (CR1) in immune complex associated with disease." Thesis, University of Oxford, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382666.

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Serra, Vincent. "Influence de l'association C3b-toxine tétanique sur la production de peptides immunogéniques." Université Joseph Fourier (Grenoble), 1998. http://www.theses.fr/1998GRE10046.

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La proteine c3 est impliquee dans de nombreux mecanismes de defense de l'organisme contre des elements etrangers pathogenes. C3 participe a la reponse immune naturelle : element clef du syteme du complement, elle intervient dans l'elimination des complexes immuns. Cette proteine participe egalement a la reponse immune specifique : son influence dans l'activation b a clairement ete etablie. Un role dans l'appretement et la presentation de l'ag a egalement ete suggere. Mon projet de recherche a vise a determiner l'influence de c3b sur la generation de peptides antigeniques de la tt au cours de l'appretement dans la cpa. Je me suis d'abord interesse a mieux definir les effets de l'association de c3b a la toxine tetanique (tt) dans la presentation par les cpa aux cellules t. Les complexes tt-c3b activent tous les clones t specifiques des epitopes p2 et p30 a des doses 100 fois moins importantes, par rapport a la tt libre. Cette meilleure efficacite de presentation des cpa ne resulte pas, dans mon systeme experimentale, d'une modification de neosynthese de molecules hla-dr ou de b7. Mon etude s'est portee dans un deuxieme temps sur l'analyse de l'influence des complexes tt-c3b sur la stabilite en sds des molecules hla-dr. L'appretement de complexes tt-c3b permet la synthese de 2 fois plus de formes hla-dr1 compactes qu'avec la tt libre. Ces resultats demontrent que la proteine c3b modifie une ou plusieurs etapes de l'appretement de l'ag qui lui est associe. La production de formes hla-dr compactes en presence de complexes tt-c3b est preferentiellement observee dans les compartiments tardifs de la voie endocytaire, de type lysosomal. Je me suis enfin efforce de determiner les sequences des peptides de la tt naturellement generes par une cpa et associes aux molecules hla-dr, ainsi que d'analyser l'influence de l'association de c3b. L'appretement des complexes tt-c3b permet de generer des epitopes t differents de ceux de la tt, dont la quantite (ou l'immunogenicite) est responsable d'une meilleure activation des clones t utilises. Ces resultats suggerent donc un role direct de c3b dans la generation des epitopes t au cours de l'appretement de la tt, en favorisant la production de peptides immunogeniques differents, capables de se lier aux molecules hla-dr et d'activer de facon plus importante les clones t specifiques.
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Kisserli, Aymric. "Distribution, rôle et régulation du CRI (CD35, récepteur pour le C3b/C4b) érythrocytaire. Analyse de dépôts érythrocytaires de fractions du complément." Reims, 2008. http://theses.univ-reims.fr/exl-doc/GED00000886.pdf.

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CR1 (CD35, récepteur pour le C3b/C4b) est une glycoprotéine transmembranaire présente sur de nombreux types cellulaires. Son rôle principal à la surface des érythrocytes (E) est le transport des complexes immuns vers le foie et la rate où ils sont éliminés. Nous avons montré que le Macaque rhésus (Macaca mulatta, MM) exprime un CR1 équivalent à celui de l’Homme en taille, en densité et réparti en bouquets. Ce CR1 présente des polymorphismes allotypiques. Il exprime aussi un CR1 plus court (CR1like, CR1L), plus abondant, plus diffus, à ancrage glycophosphatidylinositol. Nous avons décrit des polymorphismes de la région Sla de CR1 impliquée dans les phénomènes d'adhérence inter-érythrocytaire entre les E parasités par P. Falciparum et les E sains chez 12 espèces de primates. Ils ne protègent pas les E de MM contre la formation des rosettes avec des E humains parasités. Nous avons séquencé les promoteurs de CR1 et CR1L de MM (MCR1, MCR1L). AML1 activateur de CR1 humain est présent dans MCR1 mais absent de MCR1L. Ets et MZF1 sont conservés. Nous avons identifié un polymorphisme allèlique (délétion de 18 nucléotides) dans CR1L humain. Nous avons étudié le dépôt de C4d érythrocytaire (EC4d) de transplantés rénaux concomitamment à l'analyse de la biopsie du greffon. Il existe une relation entre le EC4d et le marquage diffus C4d des capillaires péritubulaires du greffon ; et entre le EC4d et les lésions histologiques retrouvées en situation de rejet aigu humoral. Le EC4d offre un intérêt pour le diagnostic et le suivi des rejets en transplantation rénale. Le mécanisme des dépôts de C4d reste à élucider. L’activation de la voie classique du complément ne semble pas impliqué
@CR1 (CD35, the C3b/C4b receptor) is a transmembrane glycoprotein found on few cell types. Erythrocyte CR1 (E-CR1) is involved in immune complex (IC) clearance in liver and spleen. The binding of IC on E is improved by cluster distribution of CR1 enabling a strong avidity multivalent binding. Rhesus macaque (Macaca mulatta) was shown to express a transmembrane E-CR1 as observed in Human (same length, density, cluster distribution). This “human-type” CR1 was characterized by allotypic polymorphisms. A shorter CR1 was also observed, called CR1like (CR1L) which was more abundant, more diffuse and glycophosphatidylinositol anchored. Polymorphisms of CR1 Sla region involved in rosetting between healthy E and P. Falciparum infected E were described in 12 primate species. E from rhesus macaque were not prevented from rosetting with human infected E by those polymorphisms. CR1 and CR1L promoters from rhesus macaque (MCR1, MCR1L) were sequenced. AML1 known as human CR1 activator was found in MCR1 but was missing in MCR1L. Ets and MZF1 were conserved. HES1 et LBP1 might downregulate MCR1 and human CR1L. An allelic polymorphism corresponding to a 18 nucleotide deletion was observed in human CR1L promoter. C4d deposition at E surface (EC4d) of patients suffering from kidney acute humoral rejection was compared with biopsy analysis and related to C4d tissue deposits. EC4d appears a promising non-invasive marker of acute humoral rejection. The mechanism of C4d deposition remains to be investigated. Complement classical pathway activation did not seem to be involved
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Soames, Candida J. "Factor H : a major complement regulatory protein." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307011.

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Books on the topic "C3b"

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Ceder, Vic. A ceder chest of C3A and C3B square dance definitions. Los Olivos, CA: V. Ceder, 1994.

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Ceder, Vic. A Ceder chest of C3A and C3B square dance definitions. Los Olivos, CA (P.O. Box 841, Los Olivos 93441-0841): Vic & Debbie Ceder, 1994.

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Edexcel, ed. Chemistry AS Level Unit Test C3b. London: Edexcel, 2001.

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Edexcel, ed. Chemistry AS Level Unit Test C3b. London: Edexcel, 2002.

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Paramaswara, Bamini. Characterization of the promoter for the human factor I (C3b/C4b inactivator) gene. Ottawa: National Library of Canada, 1998.

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Grande, Nuno. CCB vinte e cinco anos: Concurso_edício_paisagem_design_acervo = CBB twenty five years : competition_building_landscape_design_collection. Lisboa: Fundação Centro Cultural de Belém, 2018.

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America, Boy Scouts of. Cub Scout Tiger Cub handbook. Irving, Tex: Boy Scouts of America, 2001.

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Sulima, Roman. ChB. Kharʹkov: Folio, 2005.

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G, Harris Eric, ed. CB3. Mason, Ohio: South-Western, 2012.

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Updike, Ken. Original Farmall Cub and Cub Cadet. St. Paul, Minn: MBI Pub., 2005.

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Book chapters on the topic "C3b"

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Fearon, Douglas T. "The Human C3b Receptor." In Complement, 101–14. Berlin, Heidelberg: Springer Berlin Heidelberg, 1985. http://dx.doi.org/10.1007/978-3-642-82416-6_6.

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Radanova, Maria, Lubka T. Roumenina, and Vasil Vasilev. "Detection of Anti-C3b Autoantibodies by ELISA." In The Complement System, 133–39. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1016-9_13.

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Jordan, Robert W., Harold R. Duke, and Dale F. Heermann. "Spatial Variability of Water Application from Center Pivot Irrigation and Precipitation." In Proceedings of the Fourth International Conference on Precision Agriculture, 1001–10. Madison, WI, USA: American Society of Agronomy, Crop Science Society of America, Soil Science Society of America, 2015. http://dx.doi.org/10.2134/1999.precisionagproc4.c3b.

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Fearon, D. T., and J. M. Ahearn. "Complement Receptor Type 1 (C3b/C4b Receptor; CD35) and Complement Receptor Type 2 (C3d/Epstein-Barr Virus Receptor; CD21)." In Current Topics in Microbiology and Immunology, 83–98. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74977-3_5.

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Staith, John A., Winnie W. Wong, Lloyd B. Klickstein, John Weis, and Douglas T. Fearon. "Human C3b/C4b Receptor (Cr1): Isolation, Protein Sequence Analysis, and Cloning of a Partial cDNA from Human Tonsil." In Proteins, 733–39. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4613-1787-6_74.

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Wright, S. D., and S. C. Silverstein. "Regulation of the function of receptors for C3b and C3bi on human mononuclear phagocytes by receptors for other ligands." In Mononuclear Phagocytes, 183–91. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5020-7_19.

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Paccaud, J. P., and J. L. Carpentier. "Surface Distribution and Pathway of Internalization of C3b Receptors (CR1) in Human Neutrophils." In Endocytosis, 17–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-84295-5_3.

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Bredehorst, R., and C. W. Vogel. "The Central Role of Cell Surface-Deposited C3b in Complement Susceptibility of Human Melanoma Cells." In Human Melanoma, 133–50. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74496-9_11.

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Fearon, D. T., and R. M. Jack. "Regulation of expression and cell surface motility of the C3b receptor on neutrophils and monocytes." In Mononuclear Phagocytes, 157–62. Dordrecht: Springer Netherlands, 1985. http://dx.doi.org/10.1007/978-94-009-5020-7_16.

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Lutz, Hans U., Pia Stammler, Daniel Kock, and Ronald P. Taylor. "Opsonic Potential of C3b-Anti-Band 3 Complexes when Generated on Senescent and Oxidatively Stressed Red Cells or in Fluid Phase." In Advances in Experimental Medicine and Biology, 367–76. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5985-2_33.

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Conference papers on the topic "C3b"

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Bode, A. P., D. T. Miller, and S. Newman. "GENERATION OF COMPLEMENT ACTIVATION PEPTIDES DURING STORAGE OF PLATELET CONCENTRATES (PC)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644689.

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Platelets are routinely stored for transfusion at room temperature in autologous, citrated plasma. We have demonstrated previously that these conditions do not completely block activation of plasma enzyme systems, as indicated by generation of thrombin activity (Vox Sanguinis, JL1:192,1986). Here, we demonstrate the conversion of large amounts of complement factor C3 during storage of citrated PC by using radioimmunoassay quantitation of the activation peptide C3a des-Arg (Upjohn Diagnostics). Supernatant samples from stored PC and from citrated platelet-poor plasma (PPP) stored under the same conditions showed a rapid linear increase in C3a levels over time with no significant difference (paired t-test, p<0.5) between PC and PPP (see table). The values at Day 10 represent conversion of approximately 11% of the native C3. Possible effects on stored platelets of C3 conversion in the surrounding plasma include:activation of platelets by C3a des-Arg (M.Polley and R. Nachman; J.Exp.Med. 158:603, 1983) and deposition of C3b on the cell surface as "innocent bystanders" (A. Salama and C. Mueller-Eckhardt; Transfusion 25:528,1985).In contrast, <10 ng/mL C5a was found in all samples tested, representing less than 0.2%conversion of C5a.Nephelometricassay of native C5 levels in PC samples showed a slight but significant difference by a paired t-test (p=0.04) between fresh PC (mean=117 ug/mL±12.0, n=6)and P stored for 10 days(nean=108 ug/mL±9.7). Nochange in C5 levels was observed in stored PPP (106 ug/mL to 107 ug/mL). Radiolabelled monoclonal antibodies to C3 fragments showed less than 600 molecules bound per platelet. This study demonstrates for the first time the extent of complement activation in stored platelet concentrates.
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Maschio, A. Del, E. Corvazier, F. Maillet, M. Kazatchkine, and J. Maclouf. "PLATELET-DEPENDENT ACTIVATION AND AMPLIFICATION OF THE POLYMORPHONUCLEAR LEUKOCYTES LYSOSOMAL ENZYME RELEASE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644858.

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The degranulatlon of human PMNs by opsonlsed zymosan (OpZ) was studied In the presence or In the absence of platelet alone or after stimulation by thrombin. Evidence Is presented that the presence of platelets Increased the extent of the liberation of lysozyme from PMNs stimulated by OpZ with a maximal intensity when they were stimulated by thrombin. The extent of the amplification was higher when the PMNs trigger was lower (i.e. 0.5 x 108 particles/ml as compared to 3.0 x 108 particles). This effect was dependent on the platelet concentration (from 10-80 platelets/PMN). Platelets stimulated by thrombin could alsoactivate the resting PMNs with a maximum obtained ata thrombin concentration of 0.1 U/ml, corresponding to the maximal release by these cells of products stored In their granules. However, the substitution ofplatelet suspensions by the released products found In their supernatant after stimulation by thrombin, resulted In a comparable stimulation only at platelet concentrations above the ones for coincubation experiments. These findings suggest that the presence of platelets themselves or In combination with their released products are responsible for this amplification. The use of zymosan alone or coated with IgG, C3b1, C3b or OpZ did not reveal any specificity of the Inducer for this amplification suggesting that platelets and/or platelet products acted by enhancing acommon step of PMNs activation Independent of the stimulus carried by the particles. Additionally, It could be noted that the maximal effect of the amplification by platelets occurred when the level of stimulation of the PMNs alone was the weakest.
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Devine, D. V., and W. F. Rosse. "PLATELET FACTOR H REGULATES THE ACTIVITY OF THE ALTERNATIVE PATHWAY OF COMPLEMENT ON THE SURFACE OF NORMAL AND PAROXYSMAL NOCTURNAL HEMOGLOBINURIA PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643979.

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Paroxysmal nocturnal hemoglobinuria (PNH)-is frequently complicated by thrombosis. It has been suggested that the abnormal interactions of PNH platelets with complement contribute to thrombosis. Using purified complement proteins, we have previously demonstrated that the platelets from some patients with PNH do not demonstrate elevated activity of C3bBb, the alternative pathway C3 amplification enzyme complex, even though they lack the C3bBb regulatory protein, decay accelerating factor (DAF). As measured by fluorescence flow cytometry, washed platelets from both normal donors and PNH patients released the fluid phase C3bBb regulatory protein, factor H, in response to the deposition of purified complement proteins. Platelet factor H was localized to the alpha granules by immunocytochemical techniques. A quantitative radioimmunoassay demonstrated that normal platelets released 54 ± 6 ng factor H/108 platelets in response to thrombin stimulation. PNH platelets contained less factor H (22 ±7 ng/108 platelets) than normal platelets. Thrombin stimulated platelets from patients with elevated C3bBb activity released less than half of the factor H measured in detergent extracts. However, thrombin stimulated platelets from PNH patients exhibiting normal C3bBb activity released nearly all their factor H. The release of factor H from normal platelets was blocked by treating the platelets with metabolic inhibitors. In the absence of factor H release, the activity of the C3bBb complex increased three-fold. In addition, the number of molecules of 1251-factor B bound per C3b increased from 0.40 to 0.92 when factor H release was blocked. The inhibition of DAF by anti-DAF had no effect on the activity of C3bBb if factor H could be released from the platelets. However, when factor H release was blocked by treatment with metabolic inhibitors, the inhibition of DAF by anti-DAF increased the activity of C3bBb by 40%. Therefore, in the absence of DAF, platelets can regulate complement activation by the alternative pathway via the release of platelet factor H. Since factor H is an alpha granule protein, platelet release in the presence of activated complement may contribute to the occurrence of thrombosis.
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Matos, Amanda Noleto de, ADRIANO AGUIAR DA SILVA, ANDRESSA AGUIAR DA SILVA, FIRAS ABDEL KAREEM TRAIREH, and KADMIEL CÂNDIDO. "MANEJO E IMUNOPATOLOGIA DA ANEMIA HEMOLÍTICA AUTOIMUNE." In II Congresso Brasileiro de Imunologia On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/ii-conbrai/6786.

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Introdução: Anemia Hemolítica Autoimune (AHAI) é uma condição clínica em que ocorre a destruição dos eritrócitos, por conta da ligação de autoanticorpos circulantes contra antígenos de glóbulos vermelhos resultando em uma destruição via sistema completo ou sistema reticulo endotelial. Objetivo: Descrever o manejo e processo fisiopatogênico da anemia hemolítica autoimune. Metodologia: Trata-se de um estudo qualitativo de revisão bibliográfica realizado através da busca ativa nas bases de dados PUBMED, NATURE immunology e Google acadêmico de artigos publicados nos últimos 2 anos na língua portuguesa e inglesa. Resultados: A AHAI pode ser classificada com base na sua etiologia, podendo ser primária ou secundária, e temperatura sendo quente, fria ou mista. Na primária, não ocorre associação a outra doença base, já a secundária, normalmente ocorre em associação a um quadro infeccioso bem como doenças autoimunes, quadros de infecções virais ou bacterianas, uso de drogas, tumores, doenças hematológicas etc. Com base na temperatura, os anticorpos quentes do tipo IgG, reagem mais fortemente a temperatura corporal (37ºC) e há hemólise extravascular pelo sistema reticulo endotelial por células fagocíticas esplênicas, que apresentam receptores para a porção Fc dos anticorpos e também para as porções C3 e C4 do complemento. Na AHAI fria, os anticorpos são da classe IgM e reagem a temperaturas entre 4ºC e 18ºC, ocorrendo hemólise intravascular pelos macrófagos do sistema retículo endotelial e normalmente está associada a fixação do complemento, especificamente a proteína C3b. Na mista, os dois tipos de autoanticorpos coexistem. Clinicamente, pode ocorrer palidez cutânea e de mucosas, fraqueza, icterícia, taquicardia, hepatoesplenomegalia e retardo de crescimento. O diagnóstico é realizado através do teste de Coombs direto, mas outros testes, como o teste para comprovação de hemólise e citometria de fluxo, auxiliam quando o primeiro resulta negativo. O tratamento consiste em reduzir o grau de hemólise, melhorando os níveis de hemoglobina e resultando na melhora dos sintomas. No caso de AHAI secundária, deve realizar o tratamento da causa-base. Conclusão: Com base no exposto o entendimento dos processos fisiopatogênicos da AHAI, além do seu diagnóstico e tratamento traz benefícios a população por trazer informações relevantes ao seu manejo precoce e eventuais complicações.
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Detsika, M., E. Diamanti, K. Ampelakiotou, E. Jahaj, S. Tsipilis, N. Athanasiou, A. Zacharis, et al. "C3a and C5b-9 levels differentially predict COVID-19 severity and mortality." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2093.

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Poullain, Philippe, Mircea Barnaure, and Stéphanie Bonnet. "Variability Assessment of the Compressive and Tensile Strength of Fibred Earthen Composites." In 4th International Conference on Bio-Based Building Materials. Switzerland: Trans Tech Publications Ltd, 2022. http://dx.doi.org/10.4028/www.scientific.net/cta.1.612.

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Earthen composites (rammed earth, cob, adobe, daub, CEB...) are experiencing renewed interest from builders due to the many advantages of these building materials, and in particular their eco-friendliness. Nevertheless, the widespreading of these materials, as certified materials and conforming to construction standards, comes against the lack of data concerning their mechanical properties. Indeed, the literature generally gives the average values of the properties without indicating the number of specimens tested neither the distribution of the data. Yet, the mean value of the compressive strength is not enough to assess the reliability of a given earthen composite to build a wall and it would be better to indicate the value of a defined percentile (characteristic value just like with concrete composites). The aim of this paper is to analyze the data about the mechanical properties (tensile and compressive strength) obtained on different formulations of cob including natural fibres or not. The tests performed allowed to determine the probability density function and the average values, the standard deviation and the percentiles, for the various properties.
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D'Angelo, A., F. Gilardoni, V. Toschi, C. Ciminiello, E. A. Sinico, and S. Viganò D'Angelo. "REDUCED PROTEIN S ANTICOAGULANT ACTIVITY IN ESSENTIAL MIXED CRYOGLOBULINEMIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644293.

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Protein S (PS) is found in two forms in plasma, as free PS, which functions as a cofactor for activated protein C, and in e-quimolar complex with C4b-binding protein (C4b-bp), an inhibitor of the complement system. The Kd of the PS-C4b-bp interaction is one order of magnitude lower than the plasma concentration of the two proteins; thus 55-60% of total PS circulates in the bound form. Evidence has been provided that in vitro complement activation does not affect the equilibrium between PS and C4b-bp; however in patients with systemic lupus erythematosus and low C4 levels, a shift from free to bound PS has been observed. To further evaluate the relationship between complement activation and PS distribution we have measured PS and C4b-bp levels in 21 patients with essential mixed cryoglobulinemia (EMC), an autoimmune disorder characterized by cryo-precitable circulating immunocomplexes and associated with vasculitis and thrombotic episodes. EMC patients had cryocrit rangin from 1 to 66% and greatly reduced complement components (Clq: 45%, C3: 71%, C4: 15% of normal). Mean PS activity was significantly reduced inpatients as compared to the control population consisting of 20 age-and sex-matched blood donors (69%, p< 0.001). Free PS was similar in patients and controls, but total PS was lower in EMC patients (82%, p<0.05). Seven EMC patients had C4b-bp levels be low 60%. Thus, reduction of PS activity in patients with EMC is not due to reduced free PS. Cultured endothelial cells synthesize and release PS with reduced specif ic activity. In EMC patients very high levels of von Willebrand factor (313%, p< 0.001) a protein released from endothelial cells, but not of ceruplasmin, another acute phase reactant protein, were observed.In vivo release of PS from en dothelial cells might contribute to reduced PS specific activity in EMC.
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Yan, Bo, Yang Xu, Hongya Xing, Kang Xi, and H. Jonathan Chao. "CAB." In SIGCOMM'14: ACM SIGCOMM 2014 Conference. New York, NY, USA: ACM, 2014. http://dx.doi.org/10.1145/2620728.2620732.

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Fujima, Jun, Aran Lunzer, Kasper Hornbæk, and Yuzuru Tanaka. "C3W." In the 13th international World Wide Web conference. New York, New York, USA: ACM Press, 2004. http://dx.doi.org/10.1145/1013367.1013517.

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Luo, Longfei, Dingcui Yu, Liang Shi, Chuanmin Ding, Changlong Li, and Edwin H. M. Sha. "CDB." In DAC '22: 59th ACM/IEEE Design Automation Conference. New York, NY, USA: ACM, 2022. http://dx.doi.org/10.1145/3489517.3530468.

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Reports on the topic "C3b"

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Kalyan Annamalai, John Sweeten, Saqib Mukhtar, Ben Thein, Gengsheng Wei, Soyuz Priyadarsan, Senthil Arumugam, and Kevin Heflin. CO-FIRING COAL: FEEDLOT AND LITTER BIOMASS (CFB AND CLB) FUELS IN PULVERIZED FUEL AND FIXED BED BURNERS. Office of Scientific and Technical Information (OSTI), August 2003. http://dx.doi.org/10.2172/822025.

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de Kemp, E. A. Canada in 3D - National Geological Surveys Committee update report. Natural Resources Canada/CMSS/Information Management, 2023. http://dx.doi.org/10.4095/331340.

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The Canada in 3D (C3D) project (https://canada3d.geosciences.ca/), formally initiated in the spring of 2020 by the National Geological Surveys Committee (NGSC) is required to provide a working group update to all its provincial and territorial partners. There have been several informal C3D working meetings with the partners prior to the creation of the C3D Charter and there has been a hiatus in communication through the Covid-19 pandemic. To re-engage the C3D community, a video tele-conference was held on June 6th, 2022 with approximately 44 participants. There was representation and presentations of all provinces and territories with various managers, technical and scientific observers. The purpose of this compilation of presentations and discussions from this 2022 C3D-NGSC reconnection meeting is to provide activity information to all participants, and their respective organizations, highlighting current geoscience compilation and modelling efforts in 2D and 3D. The aim is to help identify opportunities for collaboration on data standards, methods, applications and best practices but with the overall goal of working toward the C3D vision, outlined in the C3D charter of an updated 2D and 3D geological map/model of Canada.
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Robson, Jennifer. The Canada Learning Bond, financial capability and tax-filing: Results from an online survey of low and modest income parents. SEED Winnipeg/Carleton University Arthur Kroeger College of Public Affairs, March 2022. http://dx.doi.org/10.22215/clb20220301.

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Previous research has identified several likely causes of eligible non-participation in the Canada Learning Bond (CLB), including awareness, financial exclusion, and administrative barriers. This study expands on that research, with a particular focus on the role of tax-filing as an administrative obstacle to accessing the CLB. I present results from an online survey of low and modest income parents (n=466) conducted in 2021. We find that, even among parents reporting they have received the CLB (46%), a majority (51%) report low confidence in their familiarity with the program, and more than one in six (17%) are unaware of the need to file tax returns to maintain eligibility for annual CLB payments. Self-reported regular tax-filing is associated with a 59% increase in the probability of accessing the CLB, even when controlling for a range of parental characteristics. This study confirms previous work by Harding and colleagues (2019) that non-filing may explain some share of eligible non-participation in education savings incentives. Tax-filing services may be an important pathway to improve CLB access. Low and modest income parents show substantial diversity in their preferred filing methods and outreach efforts cannot be concentrated in only one avenue if they are to be successful. The study also tests a small ‘nudge’ to address gaps in awareness and finds that information-only approaches to outreach are likely to have limited success, even with motivated populations.
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Damman, Dennis. Cab Heating and Cooling. Office of Scientific and Technical Information (OSTI), October 2005. http://dx.doi.org/10.2172/903061.

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Daley, Philip C. C3I Rapid Prototype Investigation. Fort Belvoir, VA: Defense Technical Information Center, January 1986. http://dx.doi.org/10.21236/ada167423.

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Garvin, L. J. Canister storage building (CSB) safety analysis report phase 3: Safety analysis documentation supporting CSB construction. Office of Scientific and Technical Information (OSTI), April 1997. http://dx.doi.org/10.2172/16912.

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Balmaseda, Magdalena A., Ronan McAdam, Simona Masina, Senan Retish, Michael Mayer, and Silvio Gualdi. Derive observable ocean climate indicators from seasonal forecast. EuroSea, 2021. http://dx.doi.org/10.3289/eurosea_d4.3.

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Guerrero, Carmen. C3G, una proteína multitarea y dual. Sociedad Española de Bioquímica y Biología Molecular, December 2015. http://dx.doi.org/10.18567/sebbmdiv_anc.2015.12.1.

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Abitbol, Maximilian H. CMB-S4 Technology Book, First Edition. Office of Scientific and Technical Information (OSTI), June 2017. http://dx.doi.org/10.2172/1414402.

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K. C. Seino. CUB DI (Deionization) column control system. Office of Scientific and Technical Information (OSTI), July 1999. http://dx.doi.org/10.2172/8368.

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