Relevant bibliographies by topics / Fc receptor-like

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'Fc receptor-like'

Author: Grafiati
Published: 4 June 2021
Last updated: 8 February 2022

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Journal articles on the topic "Fc receptor-like"

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Davis, Randall S. "Fc Receptor-Like Molecules." Annual Review of Immunology 25, no. 1 (April 2007): 525–60. http://dx.doi.org/10.1146/annurev.immunol.25.022106.141541.

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Maltais, Lois J., Ruth C. Lovering, Alexander V. Taranin, Marco Colonna, Jeffrey V. Ravetch, Riccardo Dalla-Favera, Peter D. Burrows, Max D. Cooper, and Randall S. Davis. "New nomenclature for Fc receptor–like molecules." Nature Immunology 7, no. 5 (May 2006): 431–32. http://dx.doi.org/10.1038/ni0506-431.

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Lennartz, Michelle, and James Drake. "Molecular mechanisms of macrophage Toll-like receptor–Fc receptor synergy." F1000Research 7 (January 8, 2018): 21. http://dx.doi.org/10.12688/f1000research.12679.1.

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Macrophages (MØs) are a key cell type of both the innate and the adaptive immune response and can tailor their response to prevailing conditions. To sense the host’s status, MØs employ two classes of receptors: Toll-like receptors (TLRs), which are sensors for pathogen-derived material, and Fcγ receptors (FcγRs) that are detectors of the adaptive immune response. How MØs integrate the input from these various sensors is not understood and is the focus of active study. Here, we review the recent literature on the molecular mechanisms of TLR and FcgR crosstalk and synergy, and discuss the implications of these findings. This overview suggests a multilayered mechanism of receptor synergy that allows the MØ to fine-tune its response to prevailing conditions and provides ideas for future investigation.
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Abdollahi-Roodsaz, S., M. I. Koenders, P. L. van Lent, F. A. van de Loo, and W. B. van den Berg. "Toll-like receptor 2 negatively regulates Fc receptor response in macrophages and inhibits Fc R-mediated arthritis." Annals of the Rheumatic Diseases 70, Suppl 2 (February 22, 2011): A36. http://dx.doi.org/10.1136/ard.2010.148973.2.

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Silberstein, Erica, Gabriela Dveksler, and Gerardo G. Kaplan. "Neutralization of Hepatitis A Virus (HAV) by an Immunoadhesin Containing the Cysteine-Rich Region of HAV Cellular Receptor-1." Journal of Virology 75, no. 2 (January 15, 2001): 717–25. http://dx.doi.org/10.1128/jvi.75.2.717-725.2001.

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ABSTRACT Hepatitis A virus (HAV) infects African green monkey kidney (AGMK) cells via the HAV cellular receptor-1 (havcr-1), a mucin-like type 1 integral-membrane glycoprotein of unknown natural function. The ectodomain of havcr-1 contains an N-terminal immunoglobulin-like cysteine-rich region (D1), which binds protective monoclonal antibody (MAb) 190/4, followed by an O-glycosylated mucin-like threonine-serine-proline-rich region that extends D1 well above the cell surface. To study the interaction of HAV with havcr-1, we constructed immunoadhesins fusing the hinge and Fc portion of human IgG1 to D1 (D1-Fc) or the ectodomain of the poliovirus receptor (PVR-Fc) and expressed them in CHO cells. These immunoadhesins were secreted to the cell culture medium and purified through protein A-agarose columns. In a solid-phase assay, HAV bound to D1-Fc in a concentration-dependent manner whereas background levels of HAV bound to PVR-Fc. Binding of HAV to D1-Fc was blocked by treatment with MAb 190/4 but not with control MAb M2, which binds to a tag epitope introduced between the D1 and Fc portions of the immunoadhesin. D1-Fc neutralized approximately 1 log unit of the HAV infectivity in AGMK cells, whereas PVR-Fc had no effect in the HAV titers. A similarly poor reduction in HAV titers was observed after treating the same stock of HAV with murine neutralizing MAbs K2-4F2, K3-4C8, and VHA 813. Neutralization of poliovirus by PVR-Fc but not by D1-Fc indicated that the virus-receptor interactions were specific. These results show that D1 is sufficient for binding and neutralization of HAV and provide further evidence that havcr-1 is a functional cellular receptor for HAV.
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Franco, Andrea, Bazarragchaa Damdinsuren, Tomoko Ise, Jessica Dement-Brown, Huifang Li, Satoshi Nagata, and Mate Tolnay. "Human Fc Receptor–Like 5 Binds Intact IgG via Mechanisms Distinct from Those of Fc Receptors." Journal of Immunology 190, no. 11 (April 24, 2013): 5739–46. http://dx.doi.org/10.4049/jimmunol.1202860.

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Shang, Limin, Bruno Daubeuf, Martha Triantafilou, Robin Olden, Fabien Dépis, Anne-Catherine Raby, Suzanne Herren, et al. "Selective Antibody Intervention of Toll-like Receptor 4 Activation through Fc γ Receptor Tethering." Journal of Biological Chemistry 289, no. 22 (April 15, 2014): 15309–18. http://dx.doi.org/10.1074/jbc.m113.537936.

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Silberstein, Erica, Li Xing, Willem van de Beek, Jinhua Lu, Holland Cheng, and Gerardo G. Kaplan. "Alteration of Hepatitis A Virus (HAV) Particles by a Soluble Form of HAV Cellular Receptor 1 Containing the Immunoglobulin- and Mucin-Like Regions." Journal of Virology 77, no. 16 (August 15, 2003): 8765–74. http://dx.doi.org/10.1128/jvi.77.16.8765-8774.2003.

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ABSTRACT Hepatitis A virus (HAV) infects African green monkey kidney cells via HAV cellular receptor 1 (havcr-1). The ectodomain of havcr-1 contains an N-terminal cysteine-rich immunoglobulin-like region (D1), followed by a mucin-like region that extends D1 well above the cell surface. D1 is required for binding of HAV, and a soluble construct containing D1 fused to the hinge and Fc portions of human immunoglobulin G1 (IgG1), D1-Fc, bound and neutralized HAV inefficiently. However, D1-Fc did not alter the virions. To determine whether additional regions of havcr-1 are required to trigger uncoating of HAV, we constructed D1muc-Fc containing D1 and two-thirds of the mucin-like region fused to the Fc and hinge portions of human IgG1. D1muc-Fc neutralized 10 times more HAV than did D1-Fc. Sedimentation analysis in sucrose gradients showed that treatment of HAV with 20 to 200 nM D1muc-Fc disrupted the majority of the virions, whereas treatment with 2 nM D1muc-Fc had no effect on the sedimentation of the particles. Treatment of HAV with 100 nM D1muc-Fc resulted in low-level accumulation of 100- to 125S particles. Negative-stain electron microscopy analysis revealed that the 100- to 125S particles had the characteristics of disrupted virions, such as internal staining and diffuse edges. Quantitative PCR analysis showed that the 100- to 125S particles contained viral RNA. These results indicate that D1 and the mucin-like region of havcr-1 are required to induce conformational changes leading to HAV uncoating.
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Kacskovics, Imre, Zhen Wu, Neil E. Simister, László V. Frenyó, and Lennart Hammarström. "Cloning and Characterization of the Bovine MHC Class I-Like Fc Receptor." Journal of Immunology 164, no. 4 (February 15, 2000): 1889–97. http://dx.doi.org/10.4049/jimmunol.164.4.1889.

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Li, Huifang, Jessica Dement-Brown, Pei-Jyun Liao, Ilya Mazo, Frederick Mills, Zachary Kraus, Sean Fitzsimmons, and Mate Tolnay. "Fc receptor-like 4 and 5 define human atypical memory B cells." International Immunology 32, no. 12 (August 17, 2020): 755–70. http://dx.doi.org/10.1093/intimm/dxaa053.

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Abstract Atypical memory B cells accumulate in chronic infections and autoimmune conditions, and commonly express FCRL4 and FCRL5, respective IgA and IgG receptors. We characterized memory cells from tonsils on the basis of both FCRL4 and FCRL5 expression, defining three subsets with distinct surface proteins and gene expression. Atypical FCRL4+FCRL5+ memory cells had the most discrete surface protein expression and were enriched in cell adhesion pathways, consistent with functioning as tissue-resident cells. Atypical FCRL4−FCRL5+ memory cells expressed transcription factors and immunoglobulin genes that suggest poised differentiation into plasma cells. Accordingly, the FCRL4−FCRL5+ memory subset was enriched in pathways responding to endoplasmic reticulum stress and IFN-γ. We reconstructed ongoing B-cell responses as lineage trees, providing crucial in vivo developmental context. Each memory subset typically maintained its lineage, denoting mechanisms enforcing their phenotypes. Classical FCRL4−FCRL5− memory cells were infrequently detected in lineage trees, suggesting the majority were in a quiescent state. FCRL4−FCRL5+ cells were the most represented memory subset in lineage trees, indicating robust participation in ongoing responses. Together, these differences suggest FCRL4 and FCRL5 are unlikely to be passive markers but rather active drivers of human memory B-cell development and function.
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Dissertations / Theses on the topic "Fc receptor-like"

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Decraene, Maud. "Mise en place de la réponse immunitaire orchestrée par les cellules dendritiques humaines : caractérisation et étude fonctionnelle du rôle des RFcγ." Paris 6, 2005. http://www.theses.fr/2005PA066130.

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Moody, Krishna Laroche. "Attenuation of B cell receptor-toll like receptor responses by Fc gamma receptor IIB." Thesis, 2016. https://hdl.handle.net/2144/16725.

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The pathogenesis of lupus and other autoimmune diseases driven by antibody-antigen complexes involves interactions between genetic and environmental factors. The genetic factors can be separated into factors that dysregulate adaptive immunity, innate immunity or cell death. One genetic risk factor that can affect both innate and adaptive immunity is the inhibitory Fcγ receptor, FcγRIIB. Reduced or loss of function mutations in FcγRIIB lead to an increased risk of autoimmunity. Using the murine IgG2a specific B cell receptor (BCR) transgenic (Tg) mouse, AM14, our lab discovered that delivery of nucleic acid ligands via the BCR activates B cells by dual engagement of the BCR and endosomal toll like receptors (TLR) 7 and/or 9. Mechanistic studies interrogating the role of downstream signaling effectors and intracellular trafficking in the attenuation of BCR-TLR responses by FcγRIIB were limited by our inability to deliver immune complexes (IC) to non-Tg B cells or form brightly fluorescent IC. To deliver IC to non-Tg B cells, I developed a BCR adapter (BCRAM) that delivers IC to IgM-positive B cells. To track the uptake and trafficking of IC, I developed a panel of antibodies specific for streptavidin (SA). Complexes formed with biotinylated molecules and fluorescent streptavidin could be delivered to AM14 B cells or macrophages and tracked via flow cytometry and/or confocal microscopy. BCRAM and fluorescent IC were used to understand how FcγRIIB attenuated BCR-TLR responses. I found that both DNA IC and RNA IC responses were enhanced by FcγRIIB ablation. Interestingly, a naturally-occurring somatic mutation in the Fc domain of the nucleic acid-binding antibody PL2-3 prevented regulation by FcγRIIB and reduced binding to activating FcγR. Paradoxically, I found that SHIP-1, a negative regulator activated downstream of FcγRIIB engagement, promoted BCR-TLR9 responses independent of FcγRIIB. I hypothesized that FcγRIIB attenuates BCR-TLR9 responses by interfering with sensing by the endosomal TLRs. Using a pH sensing IC, I found that engagement of FcγRIIB leads to residence of the IC in a higher pH compartment. These findings demonstrate that FcγRIIB regulates the activation of autoreactive B cells by modulating the trafficking of nucleic acid containing IC to TLR7 and TLR9 associated intracellular compartments in B cells.
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Chang, Chien-Wen, and 章茜文. "The study of mouse Fc receptor like-1 (mFcRL1) signaling." Thesis, 2010. http://ndltd.ncl.edu.tw/handle/31902770061345527774.

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碩士
國立陽明大學
微生物及免疫學研究所
98
FcRLs (Fc receptor-like molecules) are a newly found receptor family that shares homology with the classical Fc receptors. There are 8 members in humans and 6 in mice. Among these family members, hFcRL1 and mFcRL1 contain most significant homology, so we speculated that mFcRL1 may be the ortholog to hFcRL1. mFcRL1 is a transmembrane protein, and it possess two Ig-like domains in the extracellular region and one ITSM (immunoreceptor tyrosine-based switch motif) and one ITAM (immunoreceptor tyrosine-based activation motif) in the cytoplasmic region, so mFcRL1 may deliver activation signal. Our previous study showed that hFcRL1 can act as a BCR coreceptor which enhances B cell activation and proliferation. In addition, hFcRL1 can activate Grb2-ERK and PI3K-Akt signal pathways. We wanted to know whether mFcRL1 induces signaling transduction and B cell activation. To test this idea, we first converted the 3 conserved tyrosines of mFcRL1 cytoplasmic domain to phenylalanines and fused the sequence with CD32 extracellularand transmembrane domains to generate chimeric receptors. After we introduced the chimeric receptors into IIA1.6 cell line and selected stable lines, these cells were used to perform experiments. We found that the chimeric receptor was tyrosine phosphorylated after ligation, and phosphorylation was significantly disappeared in the Y281F mutant, so Y281 is the major tyrosine phosphorylation site in mFcRL1. Furthermore, chimeric receptor induced some protein phosphorylation, and a protein about the 110kDa showed obvious phosphorylation after stimulation. We next examined the effect on chimeric receptor on BCR signaling. When coligation chimeric receptor with BCR, it enhanced some of BCR-induced protein phosphorylation, but had no effects to ERK activation. In addition, chimeric receptor reduced Akt activation. In conclusion, our study suggests that mFcRL1 can induce signal transduction and it may regulate BCR signaling.
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Hsieh, Tsung-Han, and 謝宗翰. "The mechanism by which Fc Receptor Like-1(FcRL1) enhances B cell receptor-induced activation." Thesis, 2009. http://ndltd.ncl.edu.tw/handle/78316950068928613907.

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碩士
國立陽明大學
微生物及免疫學研究所
97
Fc receptor-like proteins (FcRLs) are a group of receptors that have homologous sequence to the classical Fc receptors. Eight human FcRLs have been identified: FcRL1-6, FcRLA and FcRLB. FcRL1-6 are transmembrane proteins; FcRLA and FcRLB are expressed in the cytoplasm. All FcRLs except FcRL6 are expressed by B cells. Human FcRL1 has 3 extracellular immunoglobulin-like domains, a negative charged glutamic acid in the transmembrane domain, and 2 ITAM-like motifs in the cytoplasmic region. Previous study has demonstrated that human FcRL1 is an activation receptor on B cells, and it can enhance BCR-induced activation. To study the mechanism by which human FcRL1 enhances BCR-induced activation, we first examined whether FcRL1 associates with BCR coreceptor CD19 because of the co-expression FcRL1 and CD19 in B cells. Furthermore, a glutamic acid in the transmembrane domain of FcRL1 may associate with the positive charged histidine in the transmembrane domain of CD19. Our biochemical results demonstrated that HA-FcRL1 could be specifically co-immunopreciptated with CD19, but not with an non-related surface receptor CD71 in a 293T overexpression system. In addition, neither the glutamic acid in transmembrane domain nor the intracellular region of FcRL1 was essential for the association. The partial co-localization of FcRL1 and CD19 was seen on the surface of transfected 293T cells by immunofluorescence microscopy. Our signaling analysis in B cells showed that tyrosine phosphorylation of CD19 was dramatically increased after FcRL1 co-ligation with surface IgM. Consistent with this finding, the recruitment and phosphorylation of phosphatidylinositol 3’-kinase (PI3K) was significantly enhanced by FcRL1 co-ligation. However, the total protein tyrosine phosphorylation and ERK activation were not affected. Collectively, our result suggest that FcRL1 co-ligation upregulated CD19 phosphorylation, followed by the activation of PI3K. FcRL1 may act as a co-receptor in the BCR signaling.
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Chiu, Yao-Chang, and 邱耀璋. "Characterization of the expression and function of mouse Fc receptor like-1." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/23590904074041317111.

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碩士
國立陽明大學
微生物及免疫學研究所
96
Fc receptor-like molecules (FcRLs) are newly identified receptors that shared homologous sequences with the classical Fc receptors. Six mouse FcRL genes have now been identified. Although FcRLs share homology sequences with Fc receptors, there is no evidence showing that the FcRLs bind immunoglobulins (Ig), and the function of FcRLs is still unknown. Mouse FcRL1 (mFcRL1) is a transmembrane receptor that possess two extracellular Ig-like domains, a immunoreceptor tyrosine-based activation motif (ITAM) and a immunoreceptor tyrosine-based switch motif (ITSM)-like motif in its cytoplasmic region, suggesting that mFcRL1 may be an activation receptor. Previous reports have demonstrated that the mRNA of mFcRL1 is restricted only in B cells, however, the protein expression and function of mFcRL1 are unclear. In order to characterize the expression and functions of mFcRL1, we have produced a fusion protein containing extracellular region of mFcRL1 and Fc portion of human IgG1 as an immunogen to generate rat anti-mFcRL1 monoclonal antibody (mAb) and rabbit anti-mFcRL1 polyclonal antiserum. The rabbit antiserum specifically recognized mFcRL1 but did not react with mFcRLS and mFcRL5. We have obtained 3 clones out of 960 hybridoma clones and demonstrated that the three clones: 4G12, 9C2 and 10C11 specifically recognized mFcRL1 in immunofluorescent staining. By utilizing these antibodies, we found that the mFcRL1 is a glycoprotein and has 3 isoforms, 60 kDa, 65 kDa and 70 kDa, respectively. The 65 kDa and 170 kDa are the major isoforms in mouse B cell line and primary B cells. By using 4G12 mAb, we found that the expression of mFcRL1 is limited in B lineage in the bone marrow. Its expression starts from pre-B stage and the level of mFcRL1 increases as B cells mature. In the spleen, mFcRL1 is detected on marginal zone B cells and follicular B cells but not on T cells. In peritoneal lavage cells, mFcRL1 is expressed on B1 and B2 cells but not on marcophages. We have found that neither one of mAbs 4G12 and 10C11 would stimulate B cell activation or proliferation. We will keep on screening the agonist antibody and studying the function of mFcRL1 in B cells.
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Chao, Wei-Lung, and 趙偉龍. "Construction of a Eukaryotic Recombinant DNA Expressing the Fusion Protein of Human Toll-like Receptor 2 and Fc Fragment of Immunoglobulin G." Thesis, 2008. http://ndltd.ncl.edu.tw/handle/18696940370155362171.

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碩士
東海大學
食品科學系
96
Toll-like receptor 2 (TLR2), one of TLRs that recognizes a broad range of microbial components, is a membrane receptor which is closely related to innate immunity. Fc fragment of IgG can induce the polarization towards Th1 that may help to relieve hypersensitivity. Previous studies have demonstrated that the signal transduction via membrane TLR2, was decreased by soluble TLR2 (sTLR2) in breast milk and plasma, thereby minimized the risk of allergy. In this study, we intended to express the functional sTLR2-Fc fusion protein to evaluate its potential protective role toward asthma. Full coding sequences of TLR2 was cloned to a T&A cloning vector. After trimming out the TLR2 stop codon and toll/interlukin-1 receptor, TLR2 was combined with Fc fragment which contains hinge, CH2, and CH3. The hybrid construct and wild-type TLR2 control were then subcloned to pIRES2-EGFP for eukaryotic expression in human embryo kidney cell line HEK-293, after DNA sequence verification. The estimated molecular weight of expression proteins are 87, 90, and 112 kDa. The result show that sTLR2 and Fc in breast milk consisted more than one form. Human breast milk obtained in one week and one month after childbirth contained four forms in sTLR2 ranging from 55~95 kDa, and two forms in Fc of IgG ranging from 28~72 kDa. The expressed protein wild-type TLR2 and recombined sTLR2-Fc proteins will be manifested by Western blot analysis.
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Bašus, Kryštof. "Monitorování dynamiky proteinových sítí: role FcRL proteinů při interakci membrány spermie a vajíčka." Master's thesis, 2020. http://www.nusl.cz/ntk/nusl-435880.

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Sperm-­-egg membrane interaction and fusion is mediated by various molecules of the different protein network that are located on both egg and sperm membrane. So far, many proteins have been selected to be fusion candidates, some of them (Izumo1, CD9, Juno) were proven to be essential, whereas others were discovered to play an unsuspected new active role (CD46, tetraspanins). After the adhesion of sperm to an egg, Juno located on the oolema associates with monomeric Izumo1 on sperm membrane, which is results in Izumo1 dimerization following quick removal of Juno from the egg surface as described in mouse. It implies that additional receptor on the egg membrane is required to play a role in sperm-­-egg fusion. To find a human fusogenic receptor for IZUMO1 protein we used one-­-bead-­-one-­-compound (OBOC) assay, a random screening approach. A bead, fulfilling all the requirements when interacting with the human sperm, carried a peptide sequence showing homology with the conserved Ig domain of the human specific Fc receptor-­-like protein 3 (FcRL3). In general, the ...
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Jesus, Kátia Ribeiro de. "Immunology and genetics in nonhuman primates: Study of KIR3DL02 interaction with MHC-class-I ligands of rhesus macaques." Master's thesis, 2018. http://hdl.handle.net/10316/82073.

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Dissertação de Mestrado em Investigação Biomédica apresentada à Faculdade de Medicina
Células natural killer (NK) são linfócitos capazes de matar células alvo infectadas ou transformadas por vírus. A ativação da lise de células alvo pelas células NK é mediada pelos receptores presentes nestas células. Um grupo importante de receptores são os receptores tipo imunoglobulina das células killer (KIR), sabe-se que estes ligam a membros da família polimórfica de moléculas MHC-classe-I. O macaco rhesus foi considerado um modelo animal primata não-humano de grande importância para doenças infeciosas nos humanos. Durante infecção experimental com o vírus da imunodeficiência símia (SIV), foi estabelecida uma conexão entre a presença de certos KIR e alelos MHC-classe-I com maiores ou mais baixos níveis virais, e consequentemente com uma mais rápida ou mais lenta progressão da doença. Curiosamente, foi demonstrado que a expressão de KIR3DL02 está associada com níveis virais mais baixos em animais em ensaios experimentais de infecção. Contudo, as especificações da interação entre KIR3DL02 e ligandos de MHC-classe-I são desconhecidas. O objetivo do presente trabalho, foi, por um lado, estudar a interação entre KIR3DL02 e certos alelos de Mamu, através do uso de proteínas recombinantes de KIR-Fc multimerizadas para marcar células que expressam Mamu. Para além disto, de modo a expandir o espectro de futuros estudos de interação, novos alelos de Mamu foram amplificados de cDNA de macaco rhesus e clonados em vectores de expressão de mamíferos. O trabalho aqui descrito permitiu a otimização dos estudos de ligação com o uso de proteínas KIR-Fc de fusão e células K-562 transfectadas com Mamu AcGFP. Identificação de potenciais ligandos para KIR3DL02 assim como construção de novos vectores de expressão de Mamu foram conseguidos com sucesso. Contudo, é necessária a realização de mais estudos para averiguar os resultados aqui descritos e para estudar a interação entre KIR3DL02 e os novos alelos de Mamu amplificados, com especial interesse no alelo Mamu B*008 por estar associado a um efeito protetivo.
Natural killer (NK) cells are lymphocytes that are able to kill virus infected or transformed target cells. The activation of the NK cell mediated target cell lysis is achieved by the action of NK cell receptors. An important group of receptors are the killer cell Ig-like receptors (KIR), which are known to bind members of the polymorphic family of MHC-class-I molecules. The rhesus macaque has been considered of great importance as a nonhuman primate model of human infectious diseases. During experimental simian immunodeficiency virus (SIV) infection, a connection has been established between the presence of certain KIR and MHC-class-I alleles with higher or lower viral load, and consequently to faster or slower progression of the disease. Interestingly, the expression of KIR3DL02 transcripts was shown to be associated with low viral loads and elite controller animals. However, the specificity of interaction between KIR3DL02 and MHC-class-I ligands is unknown. The aim of the present work was, for one, study the interaction between KIR3DL02 and certain Mamu alleles using multimerized KIR-Fc recombinant proteins to stain Mamu expressing cells. Additionally, in order to widen the spectrum of future interaction studies, new Mamu alleles were amplified from cDNA of rhesus macaque and cloned into a mammalian expression vector. The present work allowed the optimization of binding assays using KIR-Fc fusion proteins with K-562 Mamu AcGFP transfected cells. Identification of potential KIR3DL02 ligands as well as production of new Mamu mammalian expression constructs was accomplished. However, further studies need to be conducted to verify results here described and to study interaction between KIR3DL02 and new Mamu alleles amplified. Herein, in special, the known protective Mamu B*008 allele.
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Book chapters on the topic "Fc receptor-like"

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Ehrhardt, Götz R. A., and Max D. Cooper. "Immunoregulatory Roles for Fc Receptor-Like Molecules." In Current Topics in Microbiology and Immunology, 89–104. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/82_2010_88.

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Oleszak, Emilia L., and Julian L. Leibowitz. "Fc Receptor-Like Activity of Mouse Hepatitis Virus E2 Glycoprotein." In Advances in Experimental Medicine and Biology, 51–58. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5823-7_8.

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García-García, Erick, and Carlos Rosales. "Fc receptor signaling during phagocytosis." In Activating and Inhibitory Immunoglobulin-like Receptors, 165–74. Tokyo: Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-53940-7_21.

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Hogarth, P. Mark, Maree S. Powell, Lisa J. Harris, Bruce Wines, and Gary Jamieson. "The Fc receptor family structure based strategies for the development of anti-inflammatory drugs." In Activating and Inhibitory Immunoglobulin-like Receptors, 107–14. Tokyo: Springer Japan, 2001. http://dx.doi.org/10.1007/978-4-431-53940-7_14.

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Daëron, Marc. "Fc Receptors and Fc Receptor-Like Molecules within the Immunoreceptor Family." In Encyclopedia of Immunobiology, 360–70. Elsevier, 2016. http://dx.doi.org/10.1016/b978-0-12-374279-7.02017-8.

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N. Pramod, Siddanakoppalu. "Immunological Basis for the Development of Allergic Diseases-Prevalence, Diagnosis and Treatment Strategies." In Cell Interaction - Molecular and Immunological Basis for Disease Management. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.95804.

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Allergy is an immune disorder due to over responsiveness of immune system to a relatively normal and harmless antigen; derived from environmental and dietary substances commonly referred as allergens. Allergy is an IgE mediated type I hypersensitivity which is characterized by the degranulation of specialized white blood cells known as mast cells and basophils. Majority of characterized allergens are proteinaceous in nature and induce Th2 response. Specific Th2 cytokines elicit the induction of allergen specific IgE antibodies in sensitive individuals. The IgE binds to Fc epsilon receptor on basophil/mast cells and on exposure, allergens cross links the IgE and induce release of hypersensitivity mediators that result in allergic symptoms. The symptoms varies from mild allergies like hay fever, itchiness, rashes, rhinatisis, conjunctivitis to a severe condition such as Asthma and some time life threatening anaphylaxis. At present a various blood based test exist to diagnose allergies which include skin prick, patch test and Specific IgE tests. The best treatment available is to avoid exposure to allergens alternatively use of anti-histamines, steroids or other symptom reducing medications are in practice. Immunotherapy to desensitize the response to allergen and targeted therapy are promising for allergy in future.
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Kumar, Swatantra, Rajni Nyodu, Vimal K. Maurya, and Shailendra K. Saxena. "Pathogenesis and Host Immune Response during Japanese Encephalitis Virus Infection." In Innate Immunity in Health and Disease. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.98947.

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Abstract:
Japanese Encephalitis Virus (JEV) is a mosquito borne flavivirus infection. Transmission of JEV starts with the infected mosquito bite where human dermis layer act as the primary site of infection. Once JEV makes its entry into blood, it infects monocytes wherein the viral replication peaks up without any cell death and results in production of TNF-α. One of the most characteristics pathogenesis of JEV is the breaching of blood brain barrier (BBB). JEV propagation occurs in neurons that results in neuronal cell death as well as dissemination of virus into astrocytes and microglia leading to overexpression of proinflammatory cytokines. JEV infection results in host cells mediated secretion of various types of cytokines including type-1 IFN along with TNF-α and IFN-γ. Molecule like nitrous oxide (NO) exhibits antiviral activities against JEV infection and helps in inhibiting the viral replication by blocking protein synthesis and viral RNA and also in virus infected cells clearance. In addition, the antibody can also acts an opsonizing agent in order to facilitate the phagocytosis of viral particles, which is mediated by Fc or C3 receptor. This chapter focuses on the crucial mechanism of JEV induced pathogenesis including neuropathogenesis viral clearance mechanisms and immune escape strategies.
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Conference papers on the topic "Fc receptor-like"

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Vokac, KA, J. Ferrars, and RR Montgomery. "RISTOCETIN-INDUCED ENDOTHELIAL CELL BINDING OF PLASMA VON WILLEBRAND FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642913.

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Our laboratory previously used a technique of labeling plasma von Willebrand factor (vWf) with radiolabeled AVW1 - a “ neutral” monoclonal antibody to vWf. This technique has been used to study the binding of plasma vWf to platelets in the plasma milieu. Studies by several laboratories including ours have demonstrated structural glycoproteins on endothelial cells that are analogous to platelet GP Ilb/IIIa and we have shown that the platelet alloantigen Pl-Al is expressed on the surface of cultured endothelial cells. We undertook this study to evaluate the binding of plasma vWf to cultured endothelial cells in confluent monolayer cultures using the “ neutral” monoclonal antibody technique. Plasma vWf was “ labeled” using trace quantities of radiolabeled AVW-1. We then added 80,000 cpm of monoclonal-labeled plasma to 48 well culture plates containing confluent secondary cultures of human umbilical vein endothelial cells. Following the addition of ristocetin, the plates were incubated for 1 hour at room temperature, centrifuged, and the count8 bound and the counts remaining in the supernate were determined. In the presence of ristocetin, 67.5% of the labeled vWf bound to the endothelial cells. When “ labeled“ severe von Willebrand plasma was used or when ristocetin was omitted, less than 5% of the counts bound. Controls using mouse serum or excess mouse IgG to rule out Fc receptor binding and controls to evaluate binding to the subcellular matrix were performed and demonstrated this binding to be vWf and cell surface dependent. Unlike platelet vWf binding, this binding was not inhibited by monoclonal or polyclonal antibodies to platelet GPIb. We studied plasma from patients with type I, a variant of type I, and type Ila vWd and found normal binding with the type I plasma, but reduced binding with the type I variant plasma (14.5%) and the type Ila plasma (7.1%). AVW3, a monoclonal antibody to vWf that blocks vWf binding to platelet GPIb, blocked vWf binding to endothelial cells. Endothelial cells, like platelets, have the ability to bind plasma von Willebrand factor in the presence of ristocetin. This phenomenon occurs on the surface of endothelial cells in culture. Qualitative and quantitative reductions of this vWf binding are found with the plasma of patients with von Willebrand’s disease.
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