cryoglobulinemia/tyrosine

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Imatinib suppresses cryoglobulinemia and secondary membranoproliferative glomerulonephritis.

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Imatinib is a receptor tyrosine kinase inhibitor that blocks the activity of c-Abl, c-Kit, and PDGF receptors. We tested the protective effects of imatinib in thymic stromal lymphopoietin transgenic mice, a model of cryoglobulinemia and associated membranoproliferative glomerulonephritis (MPGN), in

Imatinib therapy for non-infection-related type II cryoglobulinemia with membranoproliferative glomerulonephritis.

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Cryoglobulinemia is a systemic immune complex-mediated vasculitis that can have significant morbidity and mortality. The current treatment for cryoglobulinemia, including chlorambucil, steroids, plasmapheresis, and rituximab, is lacking in terms of efficacy, safety, and relapse rates. Imatinib, a

Deletion of activating Fcgamma receptors does not confer protection in murine cryoglobulinemia-associated membranoproliferative glomerulonephritis.

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Many types of glomerulonephritis are initiated by the deposition of immune complexes, which induce tissue injury via either engagement of Fc receptors on effector cells or via complement activation. Four murine Fcgamma receptors (FcgammaRs) have been identified at present. Ligand binding to

Molecular mimicries between human IgG, IgM rheumatoid factor and streptococcal IgG Fc receptors.

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A monoclonal IgM rheumatoid factor (RF) from a patient with mixed essential cryoglobulinaemia was found to bind to type M15 group A streptococci with high affinity. The reaction was exerted via the antibody combining sites since it was inhibited by F(ab')2 fragments of anti-idiotypic (Id) antibodies

CD81-dependent binding of hepatitis C virus E1E2 heterodimers.

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Hepatitis C virus (HCV) is the leading cause of chronic liver disease worldwide. HCV is also the major cause of mixed cryoglobulinemia, a B-lymphocyte proliferative disorder. Direct experimentation with native viral proteins is not feasible. Truncated versions of recombinant E2 envelope proteins,

HCV NS5A protein containing potential ligands for both Src homology 2 and 3 domains enhances autophosphorylation of Src family kinase Fyn in B cells.

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Hepatitis C virus (HCV) infects B lymphocytes and induces mixed cryoglobulinemia and B cell non-Hodgkin's lymphoma. The molecular mechanism for the pathogenesis of HCV infection-mediated B cell disorders remains obscure. To identify the possible role for HCV nonstructural 5A (NS5A) protein in B

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