TLR9 responses of B cells are repressed by intravenous immunoglobulin through the recruitment of phosphatase |
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Authors: | Séité Jean-François Guerrier Thomas Cornec Divi Jamin Christophe Youinou Pierre Hillion Sophie |
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Affiliation: | a Université Européenne de Bretagne, France b Brest University Medical School Hospital, Brest, France |
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Abstract: | One 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. |
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Keywords: | Intravenous immunoglobulin B lymphocyte TLR9 Autoimmune diseases |
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