Relevant bibliographies by topics / Fc fragment

Academic literature on the topic 'Fc fragment'

Author: Grafiati
Published: 4 June 2021
Last updated: 20 February 2023

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Journal articles on the topic "Fc fragment"

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Stone, G. C., U. Sjöbring, L. Björck, J. Sjöquist, C. V. Barber, and F. A. Nardella. "The Fc binding site for streptococcal protein G is in the C gamma 2-C gamma 3 interface region of IgG and is related to the sites that bind staphylococcal protein A and human rheumatoid factors." Journal of Immunology 143, no. 2 (July 15, 1989): 565–70. http://dx.doi.org/10.4049/jimmunol.143.2.565.

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Abstract The isolated 35 kDa fragment of protein G obtained by papain digestion of group G streptococci was found to bind solid phase intact IgG, Fc (2C gamma 2 + 2C gamma 3 domains), F(ab')2 and F(acb)2 (F(ab')2 + 2C gamma 2 domains) fragments but not pFc' (2C gamma 3 domains) fragments. The level of binding to rabbit F(acb)2 and rabbit F(ab')2 fragments was similar. Protein G binding to solid phase Fc fragments was inhibited by IgG, Fc, staphylococcal protein A and its monovalent fragment D, but was enhanced by F(ab')2 fragments. Chemical modification of tyrosine but not histidine residues of IgG abrogated its ability to inhibit the binding of protein G to solid phase Fc fragments. Protein G was found to strongly inhibit the binding of a monoclonal and a polyclonal human rheumatoid factor to IgG. These findings indicate that protein G binds with separate sites to the Fc and F(ab')2 fragments of IgG, that the interaction with the Fc fragment occurs at the C gamma 2-C gamma 3 domain interface region and that tyrosine but not histidine residues in this area are likely involved. The relationship of the Fc fragment-binding site specificity of protein G to that of other microbial IgG binding proteins and human rheumatoid factors is discussed.
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Diamond, B., L. Boccumini, and B. K. Birshtein. "Site of binding of IgG2b and IgG2a by mouse macrophage Fc receptors by using cyanogen bromide fragments." Journal of Immunology 134, no. 2 (February 1, 1985): 1080–83. http://dx.doi.org/10.4049/jimmunol.134.2.1080.

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Abstract Cyanogen bromide fragments of murine IgG2b and IgG2a immunoglobulins were used to localize the sequences that are bound by specific IgG2b and IgG2a Fc receptors on murine macrophages. One fragment from the CH2 domain of IgG2b bound to the gamma 2b Fc receptor. Two fragments from IgG2a--one one from the CH2 domain, differing by only four amino acids from the homologous IgG2b fragment, and the other from the CH3 domain--specifically bound to the gamma 2a Fc receptor. In both a rosetting assay and a radioactive binding assay, these two fragments from IgG2a competed with intact IgG2a: however, they did not compete with each other. Rather, binding of the fragment from the CH3 domain of IgG2a augmented the binding of the fragment from the CH2 domain of IgG2a but not that of the homologous fragment from IgG2b. The binding of both IgG2a fragments was abolished by trypsin treatment of macrophages. These data suggest that 1) a sequence in the CH2 domain of IgG2b is sufficient for binding to the gamma 2b Fc receptor, 2) sequences from both the CH2 and CH3 domains of IgG2a bind to the gamma 2a Fc receptor, and 3) the binding of sequences from the CH3 domain of IgG2a may induce a conformational change in the gamma 2a Fc receptor that leads to enhanced binding of sequences from the CH2 domain.
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Lee, B. W., C. F. Simmons, T. Wileman, and R. S. Geha. "Intracellular cleavage of newly synthesized low affinity Fc epsilon receptor (Fc epsilon R2) provides a second pathway for the generation of the 28-kDa soluble Fc epsilon R2 fragment." Journal of Immunology 142, no. 5 (March 1, 1989): 1614–20. http://dx.doi.org/10.4049/jimmunol.142.5.1614.

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Abstract It has been reported that the 45-kDa low affinity Fc epsilon R (Fc epsilon R2) on B cells is cleaved spontaneously from the cell surface to release a 28-kDa soluble fragment (sFc epsilon R2). This study demonstrates an additional mechanism by which B cells generate this fragment. Data from 35S methionine pulse-chase experiments with the Fc epsilon R2 bearing human B lymphoblastoid cell line, RPMI 8866, and immunoprecipitations of cell lysates and culture supernatants with an Fc epsilon R2 specific mAb, mAb 25, demonstrates the existence of a cell-associated 28-kDa Fc epsilon R2 fragment. This fragment was shown by partial amino(NH2)-terminal sequence analysis to be identical to the previously described 28-kDa sFc epsilon R2. The resistance to cell treatment with trypsin indicated that it was located intracellularly. Its appearance early in the biosynthesis of the Fc epsilon R2 (within a 10-min pulse), before the Fc epsilon R2 reached the cell surface, suggested that some of this fragment was generated intracellularly. Neutralization of acidic organelles with NH4Cl inhibited the formation of this intracellular fragment, strongly suggesting that it was a produce of intracellular cleavage of the Fc epsilon R2. Finally, this 28-kDa intracellular fragment was shown to be released into the culture supernatant, suggesting an intracellular mechanism by which the cells generate sFc epsilon R2.
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Willis, H. E., B. Browder, A. J. Feister, T. Mohanakumar, and S. Ruddy. "Monoclonal antibody to human IgG Fc receptors. Cross-linking of receptors induces lysosomal enzyme release and superoxide generation by neutrophils." Journal of Immunology 140, no. 1 (January 1, 1988): 234–39. http://dx.doi.org/10.4049/jimmunol.140.1.234.

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Abstract The monoclonal antibody KuFc79 binds to a determinant on the Fc receptors (Fc gamma R) of human leukocytes. We examined the biologic effects of the interaction of this antibody with Fc gamma R on human neutrophils (PMNL). The univalent Fab fragment of KuFc79 inhibits the formation of rosettes with IgG-sensitized sheep erythrocytes by as much as 91.7%. In other experiments in which PMNL were washed after exposure to Fab of KuFc79, phagocytosis of IgG-sensitized sheep erythrocytes was inhibited by 36%. Fab fragments of other mouse IgG2b monoclonal proteins did not have these effects. When PMNL are exposed to coverslips coated with univalent Fab fragments of this antibody, the Fc gamma R are removed from the surface of the PMNL. Under these conditions, rosetting could be inhibited by 85.4%. We examined cross-linking of receptor bound monoclonal antibody or its Fab fragment by either Protein A or F(ab')2 of an anti-mouse Ig. As much as 31.7% of beta-glucuronidase, a marker for lysosomal enzymes, is specifically released by cross-linking the Fc gamma R on PMNL. The generation of O2- is also induced by specifically cross-linking Fc gamma R with Fab and anti-Fab. The data constitute the first formal demonstration that cross-linking of Fc gamma R on PMNL leads to enzyme release and superoxide generation.
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di Tommaso, Anne, Matthieu O. Juste, Zineb Lakhrif, Marie-Noëlle Mévélec, Coraline Borowczyk, Pierre Hammeni, Guillaume Désoubeaux, et al. "Engineering and Functional Evaluation of Neutralizing Antibody Fragments Against Congenital Toxoplasmosis." Journal of Infectious Diseases 224, no. 4 (August 7, 2021): 705–14. http://dx.doi.org/10.1093/infdis/jiab141.

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Abstract Maternal-fetal transmission of Toxoplasma gondii tachyzoites acquired during pregnancy has potentially dramatic consequences for the fetus. Current reference-standard treatments are not specific to the parasite and can induce severe side effects. In order to provide treatments with a higher specificity against toxoplasmosis, we developed antibody fragments—single-chain fragment variable (scFv) and scFv fused with mouse immunoglobulin G2a crystallizable fragment (scFv-Fc)—directed against the major surface protein SAG1. After validating their capacity to inhibit T. gondii proliferation in vitro, the antibody fragments’ biological activity was assessed in vivo using a congenital toxoplasmosis mouse model. Dams were treated by systemic administration of antibody fragments and with prevention of maternal-fetal transmission being used as the parameter of efficacy. We observed that both antibody fragments prevented T. gondii dissemination and protected neonates, with the scFv-Fc format having better efficacy. These data provide a proof of concept for the use of antibody fragments as effective and specific treatment against congenital toxoplasmosis and provide promising leads.
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Carosella, E. D., A. B. Tilden, and N. E. Dunlap. "Human B cell differentiation by Fc fragment." Cellular Immunology 121, no. 2 (July 1989): 269–79. http://dx.doi.org/10.1016/0008-8749(89)90025-7.

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Coe, Alexander P. F., Janet A. Askari, Adam D. Kline, Martyn K. Robinson, Hishani Kirby, Paul E. Stephens, and Martin J. Humphries. "Generation of a Minimal α5β1Integrin-Fc Fragment." Journal of Biological Chemistry 276, no. 38 (June 1, 2001): 35854–66. http://dx.doi.org/10.1074/jbc.m103639200.

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Kim, Eunhee G., Jieun Jeong, Junghyeon Lee, Hyeryeon Jung, Minho Kim, Yi Zhao, Eugene C. Yi, and Kristine M. Kim. "Rapid Evaluation of Antibody Fragment Endocytosis for Antibody Fragment–Drug Conjugates." Biomolecules 10, no. 6 (June 25, 2020): 955. http://dx.doi.org/10.3390/biom10060955.

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Antibody–drug conjugates (ADCs) have emerged as the most promising strategy in targeted cancer treatment. Recent strategies for the optimization ADCs include the development of antibody fragment–drug conjugates (FDCs). The critical factor in the successful development of ADCs and FDCs is the identification of tumor antigen-specific and internalizing antibodies (Abs). However, systematic comparison or correlation studies of internalization rates with different antibody formats have not been reported previously. In this study, we generated a panel of scFv-phage Abs using phage display technology and their corresponding scFv and scFv-Fc fragments and evaluated their relative internalization kinetics in relation to their antibody forms. We found that the relative rates and levels of internalization of scFv-phage antibodies positively correlate with their scFv and scFv-Fc forms. Our systematic study demonstrates that endocytosis of scFv-phage can serve as a predictive indicator for the assessment of Ab fragment internalization. Additionally, the present study demonstrates that endocytic antibodies can be rapidly screened and selected from phage antibody libraries prior to the conversion of phage antibodies for the generation of the conventional antibody format. Our strategic approach for the identification and evaluation of endocytic antibodies would expedite the selection for optimal antibodies and antibody fragments and be broadly applicable to ADC and FDC development.
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Morgan, E. L., M. V. Hobbs, and W. O. Weigle. "Lymphocyte activation by the Fc region of immunoglobulin. I. Role of prostaglandins in the down regulation of Fc fragment-induced polyclonal antibody production." Journal of Immunology 134, no. 4 (April 1, 1985): 2247–53. http://dx.doi.org/10.4049/jimmunol.134.4.2247.

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Abstract Fc fragment-, subfragment-, and p23-induced polyclonal antibody production are regulated by endogenous and exogenous PGE. Addition of the PG synthetase inhibitor indomethacin (IM) to murine spleen cell cultures resulted in a significant increase in the amount of Ig secreted. Moreover, addition of exogenous PGE to culture resulted in a marked suppression of IgM and IgG secretion. Splenic adherent macrophages and P388D1 cells release PGE upon stimulation with Fc fragments, subfragments, and p23. The inclusion of IM or aspirin in culture was found to abrogate the ability of Fc fragments to induce PGE release from adherent cells. These results suggest a role for PG in immune complex mediated regulation of immune responses.
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Gallagher, D. Travis, Connor V. Galvin, and Ioannis Karageorgos. "Structure of the Fc fragment of the NIST reference antibody RM8671." Acta Crystallographica Section F Structural Biology Communications 74, no. 9 (August 29, 2018): 524–29. http://dx.doi.org/10.1107/s2053230x18009834.

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As the link between antigen binding and immune activation, the antibody Fc region has received extensive structural study. In this report, the structure of the Fc fragment of the NIST IgG1 mAb (reference material 8671) is described at 2.1 Å resolution in space group P212121, with approximate unit-cell parameters a = 50, b = 80, c = 138 Å. Prior Fc structures with a wide variety of modifications are also surveyed, focusing on those in the same crystal form. To facilitate the analysis of conformations, a reference frame and a two-parameter metric are proposed, considering the CH2 domains as mobile with respect to a fixed dimeric CH3 core. Over several human Fc structures, a significant variation in Fc elbow conformations is observed, which may serve to facilitate the regulation of Fc effector signaling.
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Dissertations / Theses on the topic "Fc fragment"

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D'ACREMONT, GEFFRIER CHRISTINE. "Recepteur de faible affinite pour le fragment fc des immunoglobulines g (recepteur fc gamma de type iii) : mise en evidence de la forme soluble circulante dans le plasma humain." Nantes, 1989. http://www.theses.fr/1989NANT030M.

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Chichehian, Behrouz. "Formes solubles et membranaires des récepteurs du fragment Fc des IgG chez l'homme." Montpellier 1, 1987. http://www.theses.fr/1987MON13510.

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Benhamou, Marc. "Etude des recepteurs fc des mastocytes derives de la moelle osseuse de souris : modulation du fc::(e)r1 par la dexametasone, et caracterisation du fc::(g)r." Paris 7, 1988. http://www.theses.fr/1988PA077009.

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Bas, Mathilde. "N-glycosylation du fragment Fc : impact sur les fonctions effectrices des anticorps et sur leur pathogénicité dans l'auto-immunité du système nerveux central." Thesis, Lille 2, 2018. http://www.theses.fr/2018LIL2S055.

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Le fragment cristallisable (Fc) des immunoglobulines G (IgG) est déterminant pour leurs fonctions effectrices via sa liaison aux récepteurs au Fc (FcRs) et aux protéines du complément. La N-glycosylation portée par l’asparagine 297 (N297) du Fc impacte l’affinité de cette interaction Fc-FcRs et favorise l’engagement de FcRs aux fonctions distinctes. L’objectif de cette étude était de déterminer l’impact de la N-glycosylation du Fc sur les fonctions effectrices des anticorps et sur leur pathogénicité dans l’auto-immunité du système nerveux central (SNC).La longévité des anticorps dans la circulation sanguine dépend essentiellement de leur liaison au récepteur néonatal (FcRn) qui prévient leur dégradation. La N-glycosylation du Fc n’est généralement pas considérée comme impactant cette longévité. Cependant, nos résultats démontrent que la sialylation du Fc des anticorps est responsable d’une augmentation de leur persistance dans le sérum. Cette sialylation est permise par une mutation du Fc, une délétion d’un résidu glutamate proche de N297 dans la séquence de l’IgG1 humaine. Cet anticorps délété sialylé est également caractérisé par une perte de ses fonctions effectrices in vitro par diminution de sa liaison aux FcRs pro-inflammatoires et au complément.Nous avons étudié l’impact de la N-glycosylation du Fc sur la pathogénicité des auto-anticorps dirigés contre la myéline et qui peuvent être retrouvés dans la sclérose en plaques et la neuromyélite optique. Nous avons cloné un anticorps monoclonal pathogénique spécifique de MOG (Myelin oligodendrocyte glycoprotein) et généré des glycovariants de cette IgG1 murine par ingénierie du Fc et/ou production dans différentes lignées cellulaires. L’évaluation de leur pathogénicité dans des modèles murins d’EAE (Experimental auto-immune encephalomyelitis) a permis l’identification de variants notables. Tout d’abord, l’anticorps anti-MOG produit dans une lignée cellulaire permettant une faible fucosylation présente une pathogénicité augmentée dans l’EAE. Ensuite, l’introduction de mutations d’acides aminés spécifiques dans le Fc de l’anticorps anti-MOG, connues pour impacter la N-glycosylation, conduit à une perte de sa pathogénicité et même à une réduction de la sévérité de l’EAE induite. Une telle différence de pathogénicité entre les variants pourrait s’expliquer par des profils de liaison aux FcRs distincts.Cette étude démontre le rôle majeur de la N-glycosylation du Fc, capable de dicter la pathogénicité de la réponse anticorps dirigée contre la myéline dans les maladies auto-immunes du SNC
The crystallizable fragment (Fc) of immunoglobulins G (IgG) orchestrates their function by binding to Fc-receptors (FcRs) and complement. N-glycosylation of asparagine-297 (N297) located in the Fc domain modifies this binding affinity endowing antibodies to selectively engage functionally distinct FcRs. Here we studied the impact of Fc N-glycosylation on antibody effector functions and on their pathogenicity in central nervous system (CNS) auto-immunity.The longevity of antibodies in the blood circulation is essentially dependent on binding to the neonatal FcR (FcRn) that salvages antibodies from degradation. Fc N-glycosylation is generally excluded to impact on antibody serum persistence. Fc-sialylation might provide an exception as our results demonstrate that Fc-sialylation of antibodies enhances their persistence in the blood circulation. This polarized glycosylation is achieved using an Fc mutation, a glutamate-residue deletion at a position close to N297 in the human IgG1 sequence. The sialylated deleted antibody is also characterized by a loss of its effector functions in vitro through a reduced binding to pro-inflammatory FcRs and complement.We studied the impact of Fc N-glycosylation on the pathogenicity of myelin-reactive auto-antibodies that can be detected in multiple sclerosis and neuromyelitis optica. We cloned a pathogenic monoclonal antibody that is specific for MOG (Myelin oligodendrocyte glycoprotein) and we obtained glycovariants of this murine IgG1 by Fc-engineering and/or production in distinct cell-lines. Assessment of their pathogenicity in murine models of EAE (Experimental auto-immune encephalomyelitis) allowed identification of notable variants. First, producing the anti-MOG antibody in a hypofucosylating cell-line augments its pathogenicity in EAE. Second, introducing specific amino-acid mutations in the Fc of the anti-MOG antibody, known to impact N-glycosylation, results in a loss of its pathogenicity and even a reduced severity of induced EAE. Such a difference in the variants pathogenicity might be explained by distinct FcR-binding profiles.This study demonstrates the major potential of Fc N-glycosylation to dictate the pathogenicity of a myelin reactive antibody response during auto-immune diseases of the CNS
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Aloulou, Meryem. "La double face du signal ITAM inhibiteur (ITAMi) du système immunitaire : de la protection à l'agression." Paris 7, 2010. http://www.theses.fr/2010PA077088.

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L'homéostasie du système immunitaire est maintenue par des mécanismes finement régulés de signaux positifs et négatifs. Ils garantissent une surveillance constante pour éviter une hyperactivité du système immunitaire qui conduirait à des maladies inflammatoires et/ou. La réponse immunitaire fait intervenir des récepteurs activateurs contenant le motif ITAM (Immunoreceptors Tyrosine-based Activation Motif). Les récepteurs contenant le motif ITIM (Immunoreceptors Tyrosine-based Inhibitory Motif), dont la co-agrégation induit un signal inhibiteur suite au recrutement de phosphatases, sont l'un des mécanismes de contrôle. Dans cette étude nous avons remis en question le concept classique ITAM-ITIM en mettant en évidence les propriétés inhibitrices du motif ITAM des récepteurs RFcal et RFcvlll. Nous avons désigné cette nouvelle configuration de l'ITAM, ITAMi pour ITAM inhibiteur (Article 3). Nous avons en effet montré que la nature du ligand et sa valence étaient des éléments clés de la réponse cellulaire initiée par ces deux récepteurs. Le signal ITAMi induit par le RFcvlll lors du sepsis peut avoir des effets délétères (Article 2). En revanche, le signal ITAMi peut aussi avoir des effets bénéfiques dans certaines maladies inflammatoires ou auto-immunes (Articles 1 et 4). Le signal ITAMi des récepteurs RFcal et RFcvlll peut inhiber une variété de récepteurs cibles (tels que RFcel, TLR4, MARCO, TNFaR) en absence de co-agrégation. Néanmoins nos résultats montrent qu'au final les deux récepteurs (effecteur et cible) se retrouvent dans un même compartiment intracellulaire polarisé appelé « inhibosome » et dont la formation est essentielle à l'induction du signal ITAMi (Article 5)
Immune homeostasis is regulated by a finely tuned network of positive and negative regulatory mechanisms. These events guarantee proper surveillance and prevent hyperactivity which could lead otherwise to autoimmunity and inflammatory diseases. Immune responses involve the stimulation of immunoreceptors that contain tyrosine-based activation motifs (ITAMs). One arm of control involves immunoreceptor tyrosine-based inhibitory motif (ITIM)-bearing receptors, which, upon co-aggregation, initiate an inhibitory signal through recruitment of signal-aborting phosphatases. In this study, we have challenged the classical concept of ITAM-ITIM by highlighting the inhibitory properties of the ITAM bearing receptors FcvRIII and FcaRI. We have termed this new configuration of the ITAM, ITAMi for inhibitory ITAM (Article 3). We have shown that the type of ligand and its valency were key elaments of thé cellular response induced by both receptors. ITAMi signaling induced by RFcvlll has deleterious role during seps/s (Article 2). In contrast, ITAMi signaling may also have beneficial effects in some inflammatory or autoimmune diseases (Articles 1 and 4). ITAMi signaling induced by FcyRIII and FcaRI can inhibit signal induced by a whole variety of other receptors (such as FceRI, TLR4, MRCO, TNFaR) in thé absence of co-aggregation. Nevertheless, our results show that both receptors (effector and target) are found in the same polarized intracellular clusters named "inhibosome" whose formation is required for providing ITAMi signaling (Article 5)
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Lin, Hsin Hsin. "Mechanisms of Intravenous Immunoglobulin in the Treatment of Experimental Autoimmune Neuritis." University of Sydney, 2007. http://hdl.handle.net/2123/1696.

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The aims of this study were to test the efficacy of immunoglobulin and its Fab and Fc fragment in the treatment of experimental autoimmune neuritis (EAN) in Lewis rats, to investigate which portion of immunoglobulin is operative in the effect of IVIg, and to clarify the possible mechanisms by which immunoglobulin exerts its action in the treatment of rats EAN. EAN was induced by immunization with whole bovine peripheral nerve myelin. The immunized rats were randomized into groups, assessed clinically, electrophysiologically, and histologically, and intravenously injected with normal saline, albumin, human IVIg preparation, purified Fab or Fc fragments. The treatment efficacy was compared between normal saline and albumin groups, albumin and IVIg groups, albumin and Fab groups, albumin and Fc groups, Fab and Fc groups, Fab and IVIg groups, and Fc and IVIg groups. Methods of myelin isolation, antibody purification, and Western blot techniques were also applied. The results revealed that treatment with Fc fragment and IVIg at the onset of signs of disease effectively prevented further progression of disease, shortened disease duration, and facilitating recovery from illness as shown in clinical, electrophysiological and histological parameters. In the study which the efficacy of albumin and IVIg was compared, 5 out of 17 rats (29%) in the albumin group and 12 out of 17 (71%) in the IVIg group completely recovered from the clinical disease by day 30. The animals receiving IVIg treatment exhibited lower clinical scores, less prolongation of S wave latencies, better maintained S wave amplitudes, less reduction of distal motor NCVs, better maintained distal and proximal CMAP amplitudes, and lower histological grades. In the study which the efficacy of albumin, Fab fragment, Fc fragment, and IVIg was compared, 0 out of 8 (0%) in the albumin group, 1 out of 8 (13%) in the Fab group, 4 out of 8 (50%) in the Fc group, and 6 out of 9 (67%) rats in the IgG group completely recovered from the clinical disease by day 30. The animals receiving Fc fragment and IVIg treatment exhibited lower clinical scores, less prominent weight loss, less prolongation of S wave latencies, better maintained S wave amplitudes, less reduction of distal motor NCVs, better maintained distal and proximal CMAP amplitudes, and lower histological grades.
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Lin, Hsin Hsin. "Mechanisms of Intravenous Immunoglobulin in the Treatment of Experimental Autoimmune Neuritis." Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/1696.

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The aims of this study were to test the efficacy of immunoglobulin and its Fab and Fc fragment in the treatment of experimental autoimmune neuritis (EAN) in Lewis rats, to investigate which portion of immunoglobulin is operative in the effect of IVIg, and to clarify the possible mechanisms by which immunoglobulin exerts its action in the treatment of rats EAN. EAN was induced by immunization with whole bovine peripheral nerve myelin. The immunized rats were randomized into groups, assessed clinically, electrophysiologically, and histologically, and intravenously injected with normal saline, albumin, human IVIg preparation, purified Fab or Fc fragments. The treatment efficacy was compared between normal saline and albumin groups, albumin and IVIg groups, albumin and Fab groups, albumin and Fc groups, Fab and Fc groups, Fab and IVIg groups, and Fc and IVIg groups. Methods of myelin isolation, antibody purification, and Western blot techniques were also applied. The results revealed that treatment with Fc fragment and IVIg at the onset of signs of disease effectively prevented further progression of disease, shortened disease duration, and facilitating recovery from illness as shown in clinical, electrophysiological and histological parameters. In the study which the efficacy of albumin and IVIg was compared, 5 out of 17 rats (29%) in the albumin group and 12 out of 17 (71%) in the IVIg group completely recovered from the clinical disease by day 30. The animals receiving IVIg treatment exhibited lower clinical scores, less prolongation of S wave latencies, better maintained S wave amplitudes, less reduction of distal motor NCVs, better maintained distal and proximal CMAP amplitudes, and lower histological grades. In the study which the efficacy of albumin, Fab fragment, Fc fragment, and IVIg was compared, 0 out of 8 (0%) in the albumin group, 1 out of 8 (13%) in the Fab group, 4 out of 8 (50%) in the Fc group, and 6 out of 9 (67%) rats in the IgG group completely recovered from the clinical disease by day 30. The animals receiving Fc fragment and IVIg treatment exhibited lower clinical scores, less prominent weight loss, less prolongation of S wave latencies, better maintained S wave amplitudes, less reduction of distal motor NCVs, better maintained distal and proximal CMAP amplitudes, and lower histological grades.
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Durand, Véronique. "Etude du rôle des récepteurs de type III pour le Fc des IgG : effets regulateurs des auto-anticorps correspondants dans l'auto-immunité (doctorat : immunologie)." Brest, 2000. http://www.theses.fr/2000BRES3100.

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Krämer, Thomas [Verfasser]. "Prävention der ischämischen Querschnittlähmung durch ein carbamyliertes Fusionsprotein aus Erythropoetin und einem humanen Fc-Fragment bei Aortenokklusion am Schweinemodell / Thomas Krämer." Ulm : Universität Ulm. Medizinische Fakultät, 2013. http://d-nb.info/1030045658/34.

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Schlaeth, Martin [Verfasser]. "Untersuchung der Antikörper-abhängigen zellulären Zytotoxizität von humanisierten EGF-Rezeptor-Antikörpern mit optimiertem Antikörper-Fc-Fragment gegen Tumorzellen mit mutiertem KRAS-Protein / Martin Schlaeth." Kiel : Universitätsbibliothek Kiel, 2013. http://d-nb.info/1031190244/34.

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Book chapters on the topic "Fc fragment"

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Gooch, Jan W. "Fc Fragment." In Encyclopedic Dictionary of Polymers, 892. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13740.

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Bereli, Nilay, Handan Yavuz, and Adil Denizli. "Oriented Immobilized Anti-hIgG via Fc Fragment-Imprinted Cryogels." In Encyclopedia of Membranes, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-40872-4_732-1.

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Bereli, Nilay, Handan Yavuz, and Adil Denizli. "Oriented Immobilized Anti-hIgG via Fc Fragment-Imprinted Cryogels." In Encyclopedia of Membranes, 1435–36. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-44324-8_732.

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Renz, H., and B. Gierten. "Fc-Fragmente." In Lexikon der Medizinischen Laboratoriumsdiagnostik, 1. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-49054-9_1092-1.

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Renz, H., and B. Gierten. "Fc-Fragmente." In Springer Reference Medizin, 845. Berlin, Heidelberg: Springer Berlin Heidelberg, 2019. http://dx.doi.org/10.1007/978-3-662-48986-4_1092.

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Blundell, Patricia, and Richard Pleass. "A Method to Detect the Binding of Hyper-Glycosylated Fragment Crystallizable (Fc) Region of Human IgG1 to Glycan Receptors." In Methods in Molecular Biology, 417–21. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-8958-4_20.

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Bereli, Nilay, Handan Yavuz, and Adil Denizli. "Affinity Separation and Crystallization of Fc Fragments." In Encyclopedia of Membranes, 1–2. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-40872-4_690-1.

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Bereli, Nilay, Handan Yavuz, and Adil Denizli. "Affinity Separation and Crystallization of Fc Fragments." In Encyclopedia of Membranes, 22–23. Berlin, Heidelberg: Springer Berlin Heidelberg, 2016. http://dx.doi.org/10.1007/978-3-662-44324-8_690.

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Sádio, Flávio, Gerhard Stadlmayr, Katharina Stadlbauer, Florian Rüker, and Gordana Wozniak-Knopp. "Yeast Surface Display and Cell Sorting of Antigen-Binding Fc Fragments." In Methods in Molecular Biology, 287–308. New York, NY: Springer New York, 2019. http://dx.doi.org/10.1007/978-1-4939-9024-5_13.

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Sondermann, Peter. "Crystal Structures of Human IgG-Fc Fragments and Their Complexes with Fcγ Receptors." In Molecular and Cellular Mechanisms of Antibody Activity, 61–83. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-7107-3_3.

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Conference papers on the topic "Fc fragment"

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Kuroda, Taihei, Yutaka Abe, Akiko Kaneko, Iwasawa Yuzuru, Hideki Nariai, Hiroshi Sakaba, Kazuya Koyama, and Eiji Matsuo. "Estimation of Fragmentation on Jet Breakup in Coolant." In 2012 20th International Conference on Nuclear Engineering and the ASME 2012 Power Conference. American Society of Mechanical Engineers, 2012. http://dx.doi.org/10.1115/icone20-power2012-54399.

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Fast Breeder Reactor (FBR) is designed with safety in mind. However, there is billion to one possibility that a hypothetical Core Disruptive Accident (CDA) occurs. When CDA occurs, the Post Accident Heat Removal (PAHR) must be achieved. In the PAHR, the molten material is required to be fragmented and solidified in sodium coolant. In order to estimate whether the molten material jet is completely solidified in sodium coolant or not, it is significant to estimate jet breakup length. Although, the jet breakup length is influenced with fragmentation behavior, the correlation between them is not clear yet. Therefore, it is strongly required to clarify the mechanism of the fragmentation behavior on the jet surface. The objective of the present study is to estimate fragmentation on jet breakup in coolant experimentally. Tap water and Fluorinert™ (FC-3283) are used as simulated coolant and molten material, respectively. Flourinert is transparent and colorless liquid and its density is higher than water, therefore we can observe internal flow structure of Fluorinert. Fluorinert injected into water, and the jet breakup behavior and the fragmentation behavior of the jet are observed by using high speed video camera. In order to estimate fragmentation on liquid jet, we identified the position of the interface with back lighting technique and also, we conducted velocity measurement with Particle Image Velocimetry (PIV) technique simultaneously. It is observed that interfacial waves of the jet are generated. Waves are pulled with surrounding liquid and grown up. Finally, a fragment is separated as a droplet from front edge of the wave. Also, the vorticity is evaluated from the velocity data in order to investigate influence of the flow field in detail. From the result of calculating vorticity, the high value was estimated when jet was fragmented. It is suggested that fragmentation behavior correlates with the surrounding flow field. And the energy ratio contributing to fragmentation is calculated from velocity field. The energy ratio is important to investigate the amount of the fragmentation on liquid jet. Fragmentation on jet breakup in coolant is estimated.
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Reed, Charles, Vernon Dailey, Anissa Elayadi, Lindsay Williams, Dina Schneider, Thomas Reed, Jonathan Lewis, Richard Einstein, and Samuel Broder. "Abstract B247: Integration of a modularized protein engineering technology and the RheoSwitch Therapeutic System® platform to develop high affinity trastuzumab single chain variable fragment-Fc proteins for gene therapy applications." In Abstracts: AACR-NCI-EORTC International Conference: Molecular Targets and Cancer Therapeutics--Oct 19-23, 2013; Boston, MA. American Association for Cancer Research, 2013. http://dx.doi.org/10.1158/1535-7163.targ-13-b247.

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Pereira, J., C. Cretney, and R. H. Aster. "VARIABLE EXPRESSION OF ALLOANTIGENS IN PLATELET COHORTS OF DIFFERENT MEAN DENSITY:AN EFFECT OF AGING IN VIVO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644158.

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Platelets differ widely in size and density, but the relationship of this heterogeneity to platelet age and function is not established. Published evidence suggests that platelet alloantigens of the HLA and PlA systems may be acquired by or releasedfrom platelets in the circulation. We therefore studied expression of HLA, PlAl, and other markers in platelet cohorts of high density (HD) and low density (LD) separated on a linear, isoosmotic arabinogalactan gradient. HD and LD cohorts contained 11-14% of total platelets and did not differ significantly in mean cell volume. Alloantibodies reactive with antigens P1A1, Baka, and HLA-A2 were used to saturate alloantigen sites. Surface markers were quantified (Human Immunol. 15:251, 1986) with radiolabeled monoclonalprobes specific for HLA A, B, C antigens (W6/32), the Fc fragment of IgG (Hb-43) and the glycoprotein IIb/IIIa complex (AP-2).As shown in the Table, HD platelets carry significantly more PlAl (located on GPIIIa) and significantly less HLA than LD platelets. However, HD and LD cohorts express the same number of GPIIb/IIIa and Baka (located on GPIIb) molecules. These findings are consistent with preferential loss of HLA molecules from HD- platelets in the circulation or acquisition by LD platelets. The variable expression of P1A1 in HD and LD cohorts is apparently due to a conformational change in GPIIIa, rather than acquisition or loss of the GPIIIa molecule, because total GPIIb/IIIa was thesame in the two platelet populations. Whether antigen differences in HD and LD platelets are determined at the time of platelet production or result from aging of platelets in the circulation is under investigation.
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Mohamedali, Khalid A., Lawrence H. Cheung, Ana Alvarez-Cienfuegos, and Michael G. Rosenblum. "Abstract 2396: Development of a new generation of dimeric, highly cytotoxic fusion proteins containing active GrB and VEGF targeting tumor neovasculature: Incorporating IgG heavy chain Fc fragments improves cytotoxicity, stability and pharmacokinetics." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-2396.

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Mohamedali, Khalid A., Lawrence H. Cheung, Ana Alvarez-Cienfuegos, and Michael G. Rosenblum. "Abstract 2396: Development of a new generation of dimeric, highly cytotoxic fusion proteins containing active GrB and VEGF targeting tumor neovasculature: Incorporating IgG heavy chain Fc fragments improves cytotoxicity, stability and pharmacokinetics." In Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-2396.

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Uchiyama, Yuta, Yutaka Abe, Akiko Fujiwara, Hideki Nariai, Eiji Matsuo, Keiko Chitose, Kazuya Koyama, and Kazuhiro Itoh. "Visual Observation of Fragmentation Behavior on Molten Material Jet Surface in Coolant." In 16th International Conference on Nuclear Engineering. ASMEDC, 2008. http://dx.doi.org/10.1115/icone16-48359.

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For the safety design of the Fast Breeder Reactor (FBR), it is strongly required that the post accident heat removal (PAHR) is achieved after a postulated core disruptive accident (CDA). In the PAHR, it is important that the molten core material is solidified in sodium coolant which has high boiling point. Thus it is necessary to estimate the jet breakup length which is the distance that the molten core material is solidified in sodium coolant. In the previous studies (Abe et al., 2006), it is observed that the jet is broken up with fragmenting in water coolant by using simulated core material. It is pointed out that the jet breakup behavior is significantly influenced by the fragmentation behavior on the molten material jet surface in the coolant. However, the relation between the jet breakup behavior and fragmentation on the jet surface during a CDA for a FBR is not elucidated in detail yet. The objective of the present study is to elucidate the influence of the internal flow in the jet and fragmentation behavior on the jet breakup behavior. The Fluorinert™ (FC-3283) which is heavier than water and is transparent fluid is used as the simulant material of the core material. It is injected into the water as the coolant. The jet breakup behavior of the Fluorinert™ is observed by high speed camera to obtain the fragmentation behavior on the molten material jet surface in coolant in detail. To be cleared the effect of the internal flow of jet and the surrounding flow structure on the fragmentation behavior, the velocity distribution of internal flow of the jet is measured by PIV (Particle Image Velocimetry) technique with high speed camera. From the obtained images, unstable interfacial wave is confirmed at upstream of the jet surface, and the wave grows along the jet-water surface in the flow direction. The fragments are torn apart at the end of developed wave. By using PIV analysis, the velocity at the center of the jet is fast and it suddenly decreases near the jet surface. This means that the shear force acts on the jet and water surface. From the results of experiment, the correlation between the interfacial behavior of the jet and the generation process of fragments are discussed. In addition, the influence of surface instability of the jet induced by the relative velocity between Fluorinert™ and coolant water on the breakup behavior is also discussed.
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Modderman, P. W., J. G. Huisman, J. A. van Mourik, A. E. G. Kr, and v. d. Borne. "PLATELET ACTIVATION INDUCED BY A MONOCLONAL ANTIBODY AGAINST THE PLATELET GP Ilb/IIIa COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643514.

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A receptor for fibrinogen on the platelet GP Ila/lIIb complex is induced by ADP, thrombin and other agonists. To study functional domains on GP Ilb/IIIa, the effects of anti-GP Ilb/IIIa monoclonal antibodies (Mab’s) on platelet function were determined. One of these Mab’s, 6C9, induced platelet aggregation. The antibody binds to the intact GP Ilb/IIIa complex only, not to free GP lib or free GP Ilia. Its epitope is different from that of C17, a Mab that inhibits ADP-induced fibrinogen binding and platelet aggregation. 6C9 induces fibrinogen-mediated aggregation rather than agglutination since 6C9-induced platelet interactions were blocked by treatments that also inhibited the effects of ADP etc., without inhibiting binding of 6C9 itself. 6C9 induces binding of 125I-fibrinogen (35.000 ± 7.300 molecules/platelet, Kd = 1.3 ± 0.4 µM) to unstirred platelets. Binding of fibrinogen was 60 to 80% inhibited by apyrase, which indicates that 6C9-induced fibrinogen binding is largely mediated via ADP released from platelets. In addition, 6C9 induced aggregation of platelets in the absence of extracellular fibrinogen. Mediation of this process by platelet fibrinogen or other a-granule proteins, released upon activation by 6C9, was implicated by the finding that aggregation of washed platelets, but not of platelets to which fibrinogen was added, could be blocked by PGI2. Platelet release was also assessed directly by measuring β-thromboglobulin (α-granules) and (14C) serotonin (dense granules) in the medium of unstirred platelets incubated with 6C9. F(ab')2 fragments of 6C9 only aggregated platelets in the presence of fibrinogen and did not release (14C) serotonin. Moreover, release induced by intact 6C9 was inhibited by anti-GP Ilb/IIIa Mab C17 but not by C17 F(ab’)2, although the latter inhibited ADP-induced platelet aggregation. These data indicate that binding of antibodies to specific sites on GP Ilb/IIIa may induce Fc-dependent platelet activation.This study was supported by the Foundation for Medical Research MEDIGON (grant no. 900-526-057.
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van Dinther, T. G., F. Hol, and D. G. Meuleman. "EFFECT OF VARIOUS HEPARIN(OID)S ON HEPARIN COFACTOR II MEDIATED ANTI-THROMBIN ACTIVITY AND INHIBITION OF THROMBIN GENERATION IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644353.

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The effects of various heparin(oid)s, standard heparin VII (SH), dermatan sulphate (DS), a low molecular weight fraction of heparin (UMW-H), FragminR (FRA), Org 10172 = low molecular weight heparinoid, the fraction of Org 10172 with high affinity for AT-III (HA-10172) and the low affinity fraction (LA-10172) respectively were examined on in vitro thrombin generation and inactivation.Thrombin inactivation in the presence of either heparin cofactor II (HC-II) or anti-thrombin III (AT-III) was assessed with two newly developed assays using the purified cofactors, thrombin and chromogenic substrate S2238 on microtiterplates. Thrombin generation in the presence of HC-II and AT-III was studied using purified factor Xa, prothrombin and blood platelet lysate and the residual thrombin activity was assessed amidolytically.The inhibition of the compounds on thrombin activity are summarized in the tableThe following conclusions can be drawn:- SH, LMW-H, HA-10172 and FRA potentiate the AT-III mediated inactivation of Ha more strongly than the HC-II mediated inactivation.- DS and LA-10172 show the reverse pattern of inactivation, while Org 10172 potentiates both inactivaton pathways to a similar extent.Thrombin generation in the presence of HC-II is inhibited by mw-heparin(oid)s at approx. 2-5 times lower concentrations than the HC-II mediated thrombin inactivation, while the inhibiting effect of SH in both assays is comparable.AT-III mediated thrombin generation inhibition and AT-III mediated thrombin inactivation is comparable as well for SH, LMW-H and FRA. In contrast, Org 10172 and its subfractions are approx. 10 times more potent on AT-III mediated thrombin generation inhibition than on AT-III mediated thrombin inactivation.Org 10172 shows low anti-thrombin activity and this activity is mainly mediated via FC-II.
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Uchiyama, Yuta, Yutaka Abe, Akiko Kaneko, Hideki Nariai, Makoto Yamagishi, Eiji Matsuo, Kazuya Koyama, and Kazuhiro Itoh. "Experimental Study on Influence of Interfacial Behavior on Jet Surface Fragmentation." In 17th International Conference on Nuclear Engineering. ASMEDC, 2009. http://dx.doi.org/10.1115/icone17-75307.

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For the safety design of the Fast Breeder Reactor (FBR), it is strongly required that the Post Accident Heat Removal (PAHR) is achieved after a hypothetical Core Disruptive Accident (CDA). In the PAHR, it is important that the molten material is fragmented to be solidified by the sodium coolant with high boiling point and thermal conductivity. Furthermore, in order to estimate whether the molten material jet is completely solidified in sodium coolant or not, it is necessary to evaluate the jet breakup length. Although there are many previous studies on the jet breakup length, the tendency of jet breakup length is different for the previous studies. To estimate jet breakup length, it is necessary to understand the interaction between molten core material and coolant. The objective of the present study is to clarify the influence of the interfacial behavior of the jet on the fragmentation behavior on the jet surface. The experiments are conducted to obtain the interfacial behavior and the fragmentation behavior on the jet surface by injecting transparent Fluorinert™ (FC-3283) into water. The jet breakup behavior of the Fluorinert and the fragmentation behavior on the jet surface in pool are observed by using high speed video camera. To clarify the influence of interfacial behavior on jet surface fragmentation, it is necessary to clarify the effect of the internal flow of the jet and the surrounding flow structure on the interfacial behavior. The internal and the external velocity distribution of the jet are obtained by Particle Image Velocimetry (PIV) technique from the visual data. Shear stress is evaluated from the velocity data obtained by PIV technique. Reynolds stress and turbulent energy are also evaluated from the velocity data. As the results, shear stress becomes large along the interfacial wave. The maximum value of shear stress is decreased toward downstream. Reynolds stress becomes large at the jet surface. The vortex around the interfacial wave is observed by PIV measurement. The local shear stress acts on the interfacial wave. It is suggested that the local shear stress on the jet surface causes the fragmentation. From the experimental results, the interaction between the interfacial behavior of the jet and flow structure of the jet and surrounding fluid are discussed. The dominant mechanism of the fragmentation behavior and the influence of local shear stress at the interface on the fragementation are also discussed.
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