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Ulusoy, Canan; Kim, Eunmi; Tuzun, Erdem; Huda, Ruksana; Yilmaz, Vuslat; Poulas, Konstantinos; Trakas, Nikos; Skriapa, Lamprini; Niarchos, Athanasios; Strait, Richard T.; Finkelman, Fred D.; Turan, Selin; Zisimopoulou, Paraskevi; Tzartos, Socrates; Saruhan-Direskeneli, Guher; Christadoss, Premkumar
<?xml version='1.0' encoding='utf-8'?> <oai_dc:dc xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:oai_dc="http://www.openarchives.org/OAI/2.0/oai_dc/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/oai_dc/ http://www.openarchives.org/OAI/2.0/oai_dc.xsd"> <dc:creator>Ulusoy, Canan</dc:creator> <dc:creator>Kim, Eunmi</dc:creator> <dc:creator>Tuzun, Erdem</dc:creator> <dc:creator>Huda, Ruksana</dc:creator> <dc:creator>Yilmaz, Vuslat</dc:creator> <dc:creator>Poulas, Konstantinos</dc:creator> <dc:creator>Trakas, Nikos</dc:creator> <dc:creator>Skriapa, Lamprini</dc:creator> <dc:creator>Niarchos, Athanasios</dc:creator> <dc:creator>Strait, Richard T.</dc:creator> <dc:creator>Finkelman, Fred D.</dc:creator> <dc:creator>Turan, Selin</dc:creator> <dc:creator>Zisimopoulou, Paraskevi</dc:creator> <dc:creator>Tzartos, Socrates</dc:creator> <dc:creator>Saruhan-Direskeneli, Guher</dc:creator> <dc:creator>Christadoss, Premkumar</dc:creator> <dc:date>2014-01-01</dc:date> <dc:description>Myasthenia gravis (MG) is an autoimmune disease characterized by muscle weakness associated with acetylcholine receptor (AChR), muscle-specific receptor kinase (MuSK) or low-density lipoprotein receptor-related protein 4 (LRP4)-antibodies. MuSK-antibodies are predominantly of the non-complement fixing IgG4 isotype. The MuSK associated experimental autoimmune myasthenia gravis (EAMG) model was established in mice to investigate immunoglobulin (Ig) and cytokine responses related with MuSK immunity. C57BL/6 (B6) mice immunized with 30 mu g of recombinant human MuSK in incomplete or complete Freund's adjuvant (CFA) showed significant EAMG susceptibility (>80% incidence). Although mice immunized with 10 mu g of MuSK had lower EAMG incidence (14.3%), serum MuSK-antibody levels were comparable to mice immunized with 30 mu g MuSK. While MuSK immunization stimulated production of all antibody isotypes, non-complement fixing IgG1 was the dominant anti-MuSK Ig isotype in both sera and neuromuscular junctions. Moreover, MuSK immunized IgG1 knockout mice showed very low serum MuSK-antibody levels. Sera and MuSK-stimulated lymph node cell supernatants of MuSK immunized mice showed significantly higher levels of IL-4 and IL-10 (but not IFN-gamma and IL-12), than those of CFA immunized mice. Our results suggest that through activation of Th2-type cells, anti-MuSK immunity promotes production of IL-4, which in turn activates anti-MuSK IgG1, the mouse analog of human IgG4. These findings might provide clues for the pathogenesis of other IgG4-related diseases as well as development of disease specific treatment methods (e.g. specific IgG4 inhibitors) for MuSK-related MG. (c) 2014 Elsevier Inc. All rights reserved.</dc:description> <dc:identifier>https://aperta.ulakbim.gov.trrecord/63409</dc:identifier> <dc:identifier>oai:zenodo.org:63409</dc:identifier> <dc:rights>info:eu-repo/semantics/openAccess</dc:rights> <dc:rights>http://www.opendefinition.org/licenses/cc-by</dc:rights> <dc:source>CLINICAL IMMUNOLOGY 151(2) 155-163</dc:source> <dc:title>Preferential production of IgG1, IL-4 and IL-10 in MuSK-immunized mice</dc:title> <dc:type>info:eu-repo/semantics/article</dc:type> <dc:type>publication-article</dc:type> </oai_dc:dc>
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