PubMed:20516366 JSONTXT

{"project":"PubmedHPO","denotations":[{"id":"T1","span":{"begin":928,"end":938},"obj":"HP_0002960"},{"id":"T2","span":{"begin":928,"end":947},"obj":"HP_0002960"}],"text":"IVIg modulates BCR signaling through CD22 and promotes apoptosis in mature human B lymphocytes.\nAmong 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 G(1) phase. These changes may be accounted for the efficacy of IVIg in autoimmune diseases."}

{"project":"Allie","denotations":[{"id":"SS1_20516366_1_0","span":{"begin":152,"end":178},"obj":"expanded"},{"id":"SS2_20516366_1_0","span":{"begin":180,"end":184},"obj":"abbr"},{"id":"SS1_20516366_1_1","span":{"begin":281,"end":292},"obj":"expanded"},{"id":"SS2_20516366_1_1","span":{"begin":294,"end":296},"obj":"abbr"}],"relations":[{"id":"AE1_20516366_1_0","pred":"abbreviatedTo","subj":"SS1_20516366_1_0","obj":"SS2_20516366_1_0"},{"id":"AE1_20516366_1_1","pred":"abbreviatedTo","subj":"SS1_20516366_1_1","obj":"SS2_20516366_1_1"}],"text":"IVIg modulates BCR signaling through CD22 and promotes apoptosis in mature human B lymphocytes.\nAmong 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 G(1) phase. These changes may be accounted for the efficacy of IVIg in autoimmune diseases."}