TLR9 responses of B cells are repressed by intravenous immunoglobulin through the recruitment of phosphatase.
International audienceOne way for intravenous Ig (IVIg) to affect responses of the B cells might be to operate through their TLR7 and TLR9. We confirm the ability of TLR agonists to induce CD25 expression in B cells. For this to occur, sialylated Fc-gamma of IgG included in the IVIg preparation are required. As a result, IVIg suppresses TLR-induced production of the proinflammatory IL-6, but not that of the anti-inflammatory IL-10. That is, IVIg mimics the effects of the MyD88 inhibitor. Finally, as we previously showed that IVIg induces CD22 to recruit the inhibitory SHP-1, we established that this enzyme was also involved in IVIg-induced inhibition of TLR9 signaling. This is the first report to demonstrate such a mechanism underlying the negative impact of IVIg on B lymphocytes
MESH: Amino Acid Sequence, MESH: Autoimmune Diseases, MESH: Lymphocyte Activation, MESH: Molecular Sequence Data, MESH: Myeloid Differentiation Factor 88, MESH: Oligodeoxyribonucleotides, MESH: Protein Tyrosine Phosphatase, Non-Receptor Type 6, MESH: Reverse Transcriptase Polymerase Chain Reaction, MESH: Sialic Acid Binding Ig-like Lectin 2, MESH: Signal Transduction, MESH: Toll-Like Receptor 7, MESH: Toll-Like Receptor 9, MESH: B-Lymphocytes, MESH: Cells, Cultured, MESH: Flow Cytometry, MESH: Humans, MESH: Immunoglobulins, Intravenous, MESH: Interleukin-10, MESH: Interleukin-2 Receptor alpha Subunit, MESH: Interleukin-6, [SDV.IMM]Life Sciences [q-bio]/Immunology
Publisher: 'Elsevier BV'
DOI identifier: 10.1016/j.jaut.2011.05.014
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