IVIg-mediated amelioration of ITP in mice is dependent on sialic acid and SIGNR1.
about
Induction of Regulatory T Cells by Intravenous Immunoglobulin: A Bridge between Adaptive and Innate ImmunityA perspective on the structure and receptor binding properties of immunoglobulin G FcTranslating basic mechanisms of IgG effector activity into next generation cancer therapiesImmune recruitment or suppression by glycan engineering of endogenous and therapeutic antibodiesAnalysis and functional consequences of increased Fab-sialylation of intravenous immunoglobulin (IVIG) after lectin fractionationDeveloping the IVIG biomimetic, hexa-Fc, for drug and vaccine applicationsB cells and CD22 are dispensable for the immediate antiinflammatory activity of intravenous immunoglobulins in vivo.Cellular immune dysfunction in immune thrombocytopenia (ITP).Sweetened antibodies against humoral autoimmunity: sialylated antibodies are required for IVIg-mediated therapy.CD44 antibody-mediated amelioration of murine immune thrombocytopenia (ITP): mouse background determines the effect of FcγRIIb genetic disruption.Controlled tetra-Fc sialylation of IVIg results in a drug candidate with consistent enhanced anti-inflammatory activity.Contributions of T lymphocyte abnormalities to therapeutic outcomes in newly diagnosed patients with immune thrombocytopenia.Thymic-derived tolerizing dendritic cells are upregulated in the spleen upon treatment with intravenous immunoglobulin in a murine model of immune thrombocytopenia.Protection in antibody- and T cell-mediated autoimmune diseases by antiinflammatory IgG Fcs requires type II FcRs.Longitudinal monitoring of immunoglobulin A glycosylation during pregnancy by simultaneous MALDI-FTICR-MS analysis of N- and O-glycopeptidesSialylation converts arthritogenic IgG into inhibitors of collagen-induced arthritis.Acute inflammation primes myeloid effector cells for anti-inflammatory STAT6 signaling.A method for high-throughput, sensitive analysis of IgG Fc and Fab glycosylation by capillary electrophoresisThe challenge and promise of glycomics.Intravenous immunoglobulin-induced IL-33 is insufficient to mediate basophil expansion in autoimmune patientsFc-fusion proteins: new developments and future perspectives.The carbohydrate switch between pathogenic and immunosuppressive antigen-specific antibodies.Intravenous immunoglobulin-mediated immunosuppression and the development of an IVIG substitute.Fc glycan-modulated immunoglobulin G effector functions.Targeting B cells and autoantibodies in the therapy of autoimmune diseases.Type I and type II Fc receptors regulate innate and adaptive immunity.Intravenous immunoglobulin in neurology--mode of action and clinical efficacy.Differences in Anti-Inflammatory Actions of Intravenous Immunoglobulin between Mice and Men: More than Meets the Eye.bIgG time for large eaters: monocytes and macrophages as effector and target cells of antibody-mediated immune activation and repression.Sweet but dangerous - the role of immunoglobulin G glycosylation in autoimmunity and inflammation.Immunoglobulin Glycosylation Effects in Allergy and Immunity.Therapeutic effect of IVIG on inflammatory arthritis in mice is dependent on the Fc portion and independent of sialylation or basophils.Treatment with human immunoglobulin G improves the early disease course in a mouse model of Duchenne muscular dystrophy.Massive immune response against IVIg interferes with response against other antigens in mice: A new mode of action?Sialylation may be dispensable for reciprocal modulation of helper T cells by intravenous immunoglobulin.Pro-inflammatory State in Monoclonal Gammopathy of Undetermined Significance and in Multiple Myeloma Is Characterized by Low Sialylation of Pathogen-Specific and Other Monoclonal Immunoglobulins.Engineered Sialylation of Pathogenic Antibodies In Vivo Attenuates Autoimmune Disease.Differential antibody glycosylation in autoimmunity: sweet biomarker or modulator of disease activity?Sweet SIGNs: IgG glycosylation leads the way in IVIG-mediated resolution of inflammation.Platelet immunobiology: platelets as prey and predator
P2860
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P2860
IVIg-mediated amelioration of ITP in mice is dependent on sialic acid and SIGNR1.
description
2012 nî lūn-bûn
@nan
2012 թուականի Ապրիլին հրատարակուած գիտական յօդուած
@hyw
2012 թվականի ապրիլին հրատարակված գիտական հոդված
@hy
2012年の論文
@ja
2012年論文
@yue
2012年論文
@zh-hant
2012年論文
@zh-hk
2012年論文
@zh-mo
2012年論文
@zh-tw
2012年论文
@wuu
name
IVIg-mediated amelioration of ITP in mice is dependent on sialic acid and SIGNR1.
@ast
IVIg-mediated amelioration of ITP in mice is dependent on sialic acid and SIGNR1.
@en
type
label
IVIg-mediated amelioration of ITP in mice is dependent on sialic acid and SIGNR1.
@ast
IVIg-mediated amelioration of ITP in mice is dependent on sialic acid and SIGNR1.
@en
prefLabel
IVIg-mediated amelioration of ITP in mice is dependent on sialic acid and SIGNR1.
@ast
IVIg-mediated amelioration of ITP in mice is dependent on sialic acid and SIGNR1.
@en
P2860
P50
P356
P1476
IVIg-mediated amelioration of ITP in mice is dependent on sialic acid and SIGNR1.
@en
P2093
Inessa Schwab
P2860
P304
P356
10.1002/EJI.201142260
P407
P577
2012-04-01T00:00:00Z