Academic literature on the topic 'Lectins; Cell-cell interaction; Immunoglobulin'

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Journal articles on the topic "Lectins; Cell-cell interaction; Immunoglobulin"

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Crocker, P. "Siglecs: sialic-acid-binding immunoglobulin-like lectins in cell–cell interactions and signalling." Current Opinion in Structural Biology 12, no. 5 (October 1, 2002): 609–15. http://dx.doi.org/10.1016/s0959-440x(02)00375-5.

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Coppo, R., A. Amore, and D. Roccatello. "Dietary antigens and primary immunoglobulin A nephropathy." Journal of the American Society of Nephrology 2, no. 10 (April 1992): S173. http://dx.doi.org/10.1681/asn.v210s173.

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To investigate the role of dietary components in immunoglobulin A mesangial nephropathy (IgAGN), this study focused on gliadin, based on the reported association between coeliac disease and IgAGN as well as the pilot observation that a gluten-free diet was able to reduce the levels of circulating IgA immune complexes (IgAIC). IgA mesangial deposits in mice were induced by oral immunization with gliadin and in rats by inducing alcoholic liver cirrhosis, which increased the levels of IgA against dietary antigens (Ag). Gliadin was able to bind to cultured mesangial cells by a lectinic bond, which was reversed by competitive sugars. Binding increased mesangial cell tumor necrosis factor synthesis and decreased prostaglandin E2 production. Several gluten lectinic fractions modulate leukocyte oxidative metabolism, cytotoxicity, and chemotaxis. In IgAGN patients, serum IgA to dietary Ag were sporadically positive and IgAIC containing IgA to dietary components were significantly increased. The affinity of serum IgA to various lectins was increased in some patients. Conversely, no substantial deposition in renal tissue of dietary Ags was observed by immunofluorescence. A gluten-free diet, given to IgAGN patients with high levels of circulating IgAIC and positive antigliadin IgA, was followed by a decrease in the mean levels of both IgAIC and IgA to various dietary Ag, parallel to a reduction in proteinuria. These data suggest that dietary components, such as Ag or lectins, may play a role in IgAGN by promoting IgAIC formation and perhaps favoring mesangial localization via lectinic interactions.
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Lakhtin, V. M., M. V. Lakhtin, A. Yu Mironov, V. A. Aleshkin, and S. S. Afanasiev. "LECTIN POPULATIONS OF NK CELLS AGAINST VIRUSES-ASSOCIATED TUMORS (REVIEW OF LITERATURE)." Russian Clinical Laboratory Diagnostics 64, no. 5 (October 7, 2019): 314–20. http://dx.doi.org/10.18821/0869-2084-2019-64-5-314-320.

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Analysis of the human NK (natural killers) cells and their functionally different populations in connection to tumor processes accompanied with viral infections is presented. Receptor lectins (non-immunoglobulin proteins and their complexes recognizing polysaccharides, glycoconjugates and glycopattern-containing molecules) play important role in regulation of innate immunity. Communicative diversity of NK-cell populations (in which lectins cofunction to other receptors) is directed against tumors and viruses. Effectiveness and selectivity of action of NK cell populations can be increased in cooperation together with adaptive immunity. Evaluations of occurrence, redistribution (also under influence of cytokines) and contribution of NK-populations (depending on lectin receptors recognition coupled to multifunctions of receptors) in respect of increasing antitumor and antiviral immune responces are given. The data indicate extended prospects of lectin receptors (coupled to other type receptors) containing NK populations of the network compartment of innate immunity upon realization of different variants of organism protection in cooperation with cellular and humoral immunity. Such NK populations are the basis for further intercellular interactions. Innate immunity Cross-Talk, involving the leader NK cell populations acting according to humoral immunity mechanisms, acts on duty regime (importance for therapy of chronic pathology) that results in providing optimal combined antitumor and antiviral cytokine and cytotoxic responses according to the principle of action as «network-in-network». The influence network of lectin, Ig-like, cytotoxic, other regulator NK populations (also throuph redistribution of production of cytokines by immunocompetent cells) is perspective for forming early prolongated antitumor and antiviral processes of different types in organism. It is of importance to consider CD diversity of receptor repertuar of lectin, Ig-like and other NK populations revealing different ontogenesis as well as to seach patient key NK-populations to select and construct personally (or for contingents in cases of epidemiological significance) optimal therapeutic/prophylactic NK populations (like variants of CAR-T). Aforementioned data indicate perspectiveness of NK cell populations in development of new antitumor/antiviral effective and selective vaccine strategies, preparations and regimes of their applications. Probiotic lectins reveal features of perspective ligands cofunctioning to network of NK cell populations.
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Carlin, Aaron F., Amanda L. Lewis, Ajit Varki, and Victor Nizet. "Group B Streptococcal Capsular Sialic Acids Interact with Siglecs (Immunoglobulin-Like Lectins) on Human Leukocytes." Journal of Bacteriology 189, no. 4 (September 22, 2006): 1231–37. http://dx.doi.org/10.1128/jb.01155-06.

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ABSTRACT Group B Streptococcus (GBS) is classified into nine serotypes that vary in capsular polysaccharide (CPS) architecture but share in common the presence of a terminal sialic acid (Sia) residue. This position and linkage of GBS Sia closely resembles that of cell surface glycans found abundantly on human cells. CD33-related Siglecs (CD33rSiglecs) are a family of Sia-binding lectins expressed on host leukocytes that engage host Sia-capped glycans and send signals that dampen inflammatory gene activation. We hypothesized that GBS evolved to display CPS Sia as a form of molecular mimicry limiting the activation of an effective innate immune response. In this study, we applied a panel of immunologic and cell-based assays to demonstrate that GBS of several serotypes interacts in a Sia- and serotype-specific manner with certain human CD33rSiglecs, including hSiglec-9 and hSiglec-5 expressed on neutrophils and monocytes. Modification of GBS CPS Sia by O acetylation has recently been recognized, and we further show that the degree of O acetylation can markedly affect the interaction between GBS and hSiglec-5, -7, and -9. Thus, production of Sia-capped bacterial polysaccharide capsules that mimic human cell surface glycans in order to engage CD33rSiglecs may be an example of a previously unrecognized bacterial mechanism of leukocyte manipulation.
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Gibbons, R. J., and I. Dankers. "Immunosorbent assay of interactions between human parotid immunoglobulin A and dietary lectins." Archives of Oral Biology 31, no. 7 (1986): 477–81. http://dx.doi.org/10.1016/0003-9969(86)90022-1.

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Küppers, Ralf, and Freda K. Stevenson. "Critical influences on the pathogenesis of follicular lymphoma." Blood 131, no. 21 (May 24, 2018): 2297–306. http://dx.doi.org/10.1182/blood-2017-11-764365.

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Abstract The development of follicular lymphoma (FL) from a founder B cell with an upregulation of B-cell lymphoma 2 (BCL2), via the t(14;18) translocation, to a proliferating clone, poised to undergo further transformation to an aggressive lymphoma, illustrates the opportunistic Darwinian process of tumorigenesis. Protection against apoptosis allows an innocent cell to persist and divide, with dangerous accumulation of further mutational changes, commonly involving inactivation of chromatin-modifying genes. But this is not all. FL cells reflect normal B cells in relying on expression of surface immunoglobulin. In doing so, they add another supportive mechanism by exploiting the natural process of somatic hypermutation of the IGV genes. Positive selection of motifs for addition of glycan into the antigen-binding sites of virtually all cases, and the placement of unusual mannoses in those sites, reveals a posttranslational strategy to engage the microenvironment. A bridge between mannosylated surface immunoglobulin of FL cells and macrophage-expressed dendritic cell–specific ICAM-3–grabbing nonintegrin produces a persistent low-level signal that appears essential for life in the hostile germinal center. Early-stage FL therefore requires a triad of changes: protection from apoptosis, mutations in chromatin modifiers, and an ability to interact with lectin-expressing macrophages. These changes are common and persistent. Genetic/epigenetic analysis is providing important data but investigation of the posttranslational landscape is the next challenge. We have one glimpse of its operation via the influence of added glycan on the B-cell receptor of FL. The consequential interaction with environmental lectins illustrates how posttranslational modifications can be exploited by tumor cells, and could lead to new approaches to therapy.
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Sokal, Izabela, Agata Kułacz, Wojciech Gorczyca, Maria Janusz, and Jozef Lisowski. "Guinea pig peritoneal macrophages. Differential effects of lectins on interaction with IgG immunoglobulins." Cell Biochemistry and Function 13, no. 1 (March 1995): 25–30. http://dx.doi.org/10.1002/cbf.290130107.

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Odabashian, Mariette, Emanuela Carlotti, Shamzah Araf, Jessica Okosun, Filomena Spada, John G. Gribben, Francesco Forconi, Freda K. Stevenson, Mariarita Calaminici, and Sergey Krysov. "IGHV sequencing reveals acquired N-glycosylation sites as a clonal and stable event during follicular lymphoma evolution." Blood 135, no. 11 (March 12, 2020): 834–44. http://dx.doi.org/10.1182/blood.2019002279.

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Abstract Follicular lymphoma B cells undergo continuous somatic hypermutation (SHM) of their immunoglobulin variable region genes, generating a heterogeneous tumor population. SHM introduces DNA sequences encoding N-glycosylation sites asparagine-X-serine/threonine (N-gly sites) within the V-region that are rarely found in normal B-cell counterparts. Unique attached oligomannoses activate B-cell receptor signaling pathways after engagement with calcium-dependent lectins expressed by tissue macrophages. This novel interaction appears critical for tumor growth and survival. To elucidate the significance of N-gly site presence and loss during ongoing SHM, we tracked site behavior during tumor evolution and progression in a diverse group of patients through next-generation sequencing. A hierarchy of subclones was visualized through lineage trees based on SHM semblance between subclones and their discordance from the germline sequence. We observed conservation of N-gly sites in more than 96% of subclone populations within and across diagnostic, progression, and transformation events. Rare N-gly-negative subclones were lost or negligible from successive events, in contrast to N-gly-positive subclones, which could additionally migrate between anatomical sites. Ongoing SHM of the N-gly sites resulted in subclones with different amino acid compositions across disease events, yet the vast majority of resulting DNA sequences still encoded for an N-gly site. The selection and expansion of only N-gly-positive subclones is evidence of the tumor cells’ dependence on sites, despite the changing genomic complexity as the disease progresses. N-gly sites were gained in the earliest identified lymphoma cells, indicating they are an early and stable event of pathogenesis. Targeting the inferred mannose-lectin interaction holds therapeutic promise.
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Rodrigues Mantuano, Natalia, Marina Natoli, Alfred Zippelius, and Heinz Läubli. "Tumor-associated carbohydrates and immunomodulatory lectins as targets for cancer immunotherapy." Journal for ImmunoTherapy of Cancer 8, no. 2 (October 2020): e001222. http://dx.doi.org/10.1136/jitc-2020-001222.

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During oncogenesis, tumor cells present specific carbohydrate chains that are new targets for cancer immunotherapy. Whereas these tumor-associated carbohydrates (TACA) can be targeted with antibodies and vaccination approaches, TACA including sialic acid-containing glycans are able to inhibit anticancer immune responses by engagement of immune receptors on leukocytes. A family of immune-modulating receptors are sialic acid-binding Siglec receptors that have been recently described to inhibit antitumor activity mediated by myeloid cells, natural killer cells and T cells. Other TACA-binding receptors including selectins have been linked to cancer progression. Recent studies have shown that glycan-lectin interactions can be targeted to improve cancer immunotherapy. For example, interactions between the immune checkpoint T cell immunoglobulin and mucin-domain containing-3 and the lectin galectin-9 are targeted in clinical trials. In addition, an antibody against the lectin Siglec-15 is being tested in an early clinical trial. In this review, we summarize the previous and current efforts to target TACA and to inhibit inhibitory immune receptors binding to TACA including the Siglec-sialoglycan axis.
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Séïté, Jean-François, Divi Cornec, Yves Renaudineau, Pierre Youinou, Rizgar A. Mageed, and Sophie Hillion. "IVIg modulates BCR signaling through CD22 and promotes apoptosis in mature human B lymphocytes." Blood 116, no. 10 (September 9, 2010): 1698–704. http://dx.doi.org/10.1182/blood-2009-12-261461.

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Abstract Among various mechanisms for interactions with B cells, intravenous immunoglobulin (IVIg) may operate through the insertion of its Fc part into the Fc-γ receptor, or the binding of its sialic acid (SA)–bearing glycans to the negatively regulating CD22 lectin. It appeared that IVIg reduces B lymphocyte viability in a dose- and time-dependent manner. Furthermore, we show by confocal microscopy that SA-positive IgG, but not SA-negative IgG bind to CD22. This interaction reduces the strength of B-cell receptor–mediated signaling trough down-regulating tyrosine phosphorylation of Lyn and the B-cell linker proteins, and up-regulating phospholipase Cγ2 activation. This cascade resulted in a sustained activation of Erk 1/2 and arrest of the cell cycle at the G1 phase. These changes may be accounted for the efficacy of IVIg in autoimmune diseases.
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Dissertations / Theses on the topic "Lectins; Cell-cell interaction; Immunoglobulin"

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Vinson, Mary. "Structural and functional studies on sialoadhesin." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362115.

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Ding, Cheng. "Siglec-G is a negative regulator of NF-[kappa]B activation and has pivotal roles in B-1 cell development and resistance to sepsis /." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1226876722.

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Wilkins, Simon. "Lectin-carbohydrate mediated interaction between Plasmodium ookinetes and the mosquito midgut." Thesis, Imperial College London, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367836.

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Aigal, Sahaja [Verfasser], and Winfried [Akademischer Betreuer] Römer. "Elucidation of the host cell membrane associated interaction partners of Pseudomonas aeruginosa and its lectins (in space and time)." Freiburg : Universität, 2018. http://d-nb.info/1202438172/34.

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Agarwal, Vaibhav. "Role of PspC interaction with human polymeric immunoglobulin receptor and Factor H in Streptococcus pneumoniae infections and host cell induced signalling." kostenfrei, 2008. http://www.opus-bayern.de/uni-wuerzburg/volltexte/2009/3652/.

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Agarwal, Vaibhav [Verfasser]. "Role of PspC interaction with human polymeric immunoglobulin receptor and factor H in Streptococcus pneumoniae infections and host cell induced signalling / vorgelegt von Vaibhav Agarwal." 2008. http://d-nb.info/999468650/34.

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Hu, Ching Chih, and 胡瀞之. "Memory Regulatory T cells Increase Only In Inflammatory Phase of Chronic Hepatitis B Infection and Related to Galectin-9/T-cell Immunoglobulin and Mucin Domain-3 interaction." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/2hrca6.

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博士
長庚大學
臨床醫學研究所
106
CD4+Foxp3+ regulatory T cells are the main immune suppressors with subpopulation of inflamed-tissue related memory regulatory T cells and non-related resting regulatory T cells. Previously, regulatory T cell was proposed to be the cause of chronicity of hepatitis B virus infection but with controversies. We enrolled 124 chronically HBV infected patients and 38 healthy volunteers into the present study and investigated the role of memory regulatory T cells in four distinct immune phases of chronic HBV infection, especially the non-inflammatory versus inflammatory phases. It was found memory regulatory T cells but not resting regulatory T cells increased only in the inflammatory phase and correlated with serum alanine aminotransferase level. These memory regulatory T cells accumulated in the inflamed liver, expressed significantly higher T-cell Immunoglobulin and Mucin Domain-3 (Tim-3), CCR4 and CCR5 and fewer CCR7, and possessed potent suppressive function. These memory regulatory T cells mainly originated from natural regulatory T cells because of high Helios expression. Hierarchical clustering analysis showed higher frequency of memory regulatory T cells was concordant with higher serum alanine aminotransferase and galectin-9 levels. Furthermore, galectin-9 could expand memory regulatory T cells through galectin-9/ Tim-3 interaction. In conclusion, increased memory regulatory T cells are found only in inflammatory phase of chronic HBV infection. Galectin-9, associated with liver inflammation, contributes to the expansion of memory regulatory T cells through galectin-9/ Tim-3 interaction. Therefore, this expansion of memory regulatory T cells only reflects as an immune regulatory mechanism to limit the on-going liver damages rather than the cause of chronicity of HBV infection.
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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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Books on the topic "Lectins; Cell-cell interaction; Immunoglobulin"

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Carbohydrate recognition: Biological problems, methods, and applications. Hoboken, N.J: Wiley, 2011.

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C, Lee Y., and Lee Reiko T, eds. Recognition of carbohydrates in biological systems: Edited by Yuan C. Lee, Reiko T. Lee. San Diego, Calif: Academic Press, 2003.

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Lee, Y. C., and Reiko T. Lee. Recognition of Carbohydrates in Biological Systems, Part A : General Procedures, Volume 362 (Methods in Enzymology). Academic Press, 2003.

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Lee, Y. C., and Reiko T. Lee. Recognition of Carbohydrates in Biological Systems, Part A : General Procedures, Volume 362 (Methods in Enzymology). Academic Press, 2003.

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Book chapters on the topic "Lectins; Cell-cell interaction; Immunoglobulin"

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Sinowatz, F., E. Toepfer-Petersen, and H. J. Gabius. "Fertilization: A model for cell-cell interaction." In Lectins and Cancer, 293–304. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76739-5_22.

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Gabius, S., S. S. Joshi, J. G. Sharp, and H. J. Gabius. "Tumor cell-bone marrow stromal cell interaction: Neoglycoproteins as tools in leukemia research." In Lectins and Cancer, 273–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76739-5_20.

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Racaniello, Vincent R., Eric G. Moss, Gerardo Kaplan, and Ruibao Ren. "Interaction of Poliovirus with its Immunoglobulin-like Cell Receptor." In Microbial Adhesion and Invasion, 59–67. New York, NY: Springer New York, 1992. http://dx.doi.org/10.1007/978-1-4612-2924-7_5.

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Nakaya, Mako, Hirofumi Tachibana, and Koji Yamada. "17BETA-ESTRADIOL regulates immunoglobulin M production through interaction with estrogen receptors." In Animal Cell Technology: Basic & Applied Aspects, 239–46. Dordrecht: Springer Netherlands, 2006. http://dx.doi.org/10.1007/1-4020-4457-7_33.

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Burton, D. R. "The Molecular Basis of the Interaction of Immunoglobulin G with Complement and Phagocytic Cells." In Bacteria, Complement and the Phagocytic Cell, 91–108. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-85718-8_8.

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"A5.Membrane Lectins as Adhesion Receptors." In Glycans in Cell Interaction and Recognition, 94–106. CRC Press, 2002. http://dx.doi.org/10.4324/9780203304549-12.

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"B5: Neuropathologies involving endogeneous lectins and thier ligands." In Glycans in Cell Interaction and Recognition, 199–236. CRC Press, 2002. http://dx.doi.org/10.4324/9780203304549-18.

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Kumar Chatterjee, Swapan, and Snigdha Saha. "Glycan and Its Role in Combating COVID-19." In Biotechnology to Combat COVID-19 [Working Title]. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.97240.

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Newly identified beta-coronavirus i.e. the 2019 novel coronavirus is associated with a contagious transmittable respiratory disease called COVID-19. This disease has been declared as a “pandemic” by the World Health Organization (WHO). The entry of coronavirus in the human respiratory epithelial cells depends upon the interaction between host cell receptor ACE2 and viral S-glycoprotein. However, this type of molecular recognition in between cell surface receptors and envelope glycoproteins are mediated by specific glycan epitopes and attribute to viral entry through membrane fusion. Glycans are essential biomolecules made by all living organisms, have roles in serving structure, energy storage, and system regulatory purposes. The glycan shield plays a crucial role in concealing the surface S protein from molecular recognition. The immunomodulatory properties of Glycan-binding proteins (GBPs) like Lectins, build them as an attractive candidates for vaccine adjuvant. Investigations involving the complement system activation by the lectin pathway in COVID-19 and diseases are in need of the hour. The innate immune response involving complement system could have varied biological effects against an array of microbial infections. The advances in glycoprotein style methods especially immunomodulatory action of some lectins are necessary to boost the effectiveness of treatment of COVID-19 and other pandemics.
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D. Maniero, Gregory. "Evolutionary Conservation of the Role of CD4 as a Receptor for Interleukin-16." In Interleukins - The Immune and Non-Immune Systems’ Related Cytokines. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96951.

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The interaction of CD4 with MHC class II during helper T-cell activation and effector function is required for the initiation of an adaptive immune response in all gnathostomes. CD4 is comprised of four immunoglobulin domains but most likely arose from an ancestral two-domain homolog. The distal, D1 domain of CD4 binds to non-polymorphic regions of the MHC molecule, but despite the absolute requirement for this interaction, the sequence and structure of this domain are not well conserved through phylogeny. Conversely, the proximal, D4 domain of CD4 contains the binding site of the cytokine IL-16 and is highly conserved in its amino acid structure. IL-16 is a cytokine that has been described in a wide variety of invertebrate and vertebrate species. The CD4-binding residues on IL-16 are highly conserved throughout phylogeny, allowing for promiscuous binding of IL-16 to CD4 between members of unrelated taxa. This chapter aims to present structural, and functional support for the hypothesis that the CD4 co-receptor of the TCR arose from a primordial receptor for IL-16.
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Conference papers on the topic "Lectins; Cell-cell interaction; Immunoglobulin"

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Grabowski, E. F., and K. McKenny. "CHARACTERIZATION OF DISORDERS OF PLATELET-VESSEL WALL INTERACTION IN AN AGGREGOMETER INCORPORATING BLOOD FLOW PAST AN ENDOTHELIAL CELL MONOLAYER." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644537.

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Epi-fluorescence videomicroscopy permits real-time imaging of platelet (plt) adhesion-aggregation to a defined microinjury site of an endothelial cell monolayer (ECM) exposed to flowing blood. The fluorescent label is the TAB murine monoclonal antibody (courtesy of Dr. R.P. McEver) directed against human pit cp HB, together with a fluorescein-conjugated goat F(ab')2 against murine immunoglobulin. The combination assures specificity for pit membranes, yet leaves pit function intact. Bovine aortic ECM, grown on rectangular cover glasses, comprise one wall of a flow chamber mounted on a vertical microscope stage. A 6-0 sterile suture, drawn across the ECM in a direction transverse to flow, creates microinjuries of width 70 ± 15 (mean ± SD). Pit deposition is virtually absent upon intact and confluent regions of the ECM. On microinjury sites and at a shear rate of 270 sec-1, however, computer-enhanced images show pit adherence, aggregation, and embolization. Pretreatment of the ECM with 1.0 mMFC lysine acetyl salicylate, further, leads to a three-fold increase in aggregate length. ECM products inhibitable by aspirin, therefore, modulate adhesion-aggregation in disease and normal states under physiologic flow conditions. The Table shows that nercent coverage of the injury area, and mean aggregate length readily discriminate normal, post-aspirin, and von Willebrand's (vWD's) bloods. Aggregate length is reduced in vWD's blood to a greater degree (p<0.01) than by oral aspirin, while the latter is associated with a paradoxic increase (p<0.01) in single plt adhesion.
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