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IVIg modulates BCR signaling through CD22 and promotes apoptosis in mature human B lymphocytes

Jean-François Séïté1, Divi Cornec, Yves Renaudineau

  • 1EA2216 Immunology and Pathology and Institut Fédératif de Recherche 148, Université de Bretagne Occidentale, Brest, France.

Blood
|June 3, 2010
PubMed

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 G(1) phase. These changes may be accounted for the efficacy of IVIg in autoimmune diseases.

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