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Intravenous Immunoglobulin Therapy Affects T Regulatory Cells by Increasing Their Suppressive Function

Aharon Kessel^*, Hana Ammuri^*, Regina Peri^*, Elsa R. Pavlotzky^*, Miri Blank, Yehuda Shoenfeld and Elias Toubi^1,*

^* Division of Clinical Immunology, Bnai-Zion Medical Centre, Rappaport Faculty of Medicine, Technion, Haifa, Israel; and Department of Medicine B and Centre for Autoimmune Diseases, Chaim Sheba Medical Centre, Tel-Hashomer, Incumbent of the Laura Schwarz Kipp Chair for Research of Autoimmune Diseases, Sackler Faculty of Medicine, Tel-aviv, Israel

Intravenous Ig therapy (IVIg) is reported to be a useful regimen in treating autoimmune diseases. In this study, we asked whether IVIg (in vitro) could increase the expression of TGF-, IL-10, and the transcription factor FoxP3 in T regulatory (Treg) cells, and the idea that IVIg could enhance suppressive properties of these cells. CD4⁺ T cells from 12 healthy individuals were cultured in the presence or absence of IVIg vs human control IgG during 16, 24, and 36 h. Using FACS analysis and gating on CD4⁺CD25^high Treg cells, we assessed the expression of intracellular TGF-, IL-10, and FoxP3. In addition, the production of TNF- by stimulated CD4⁺ T cells alone or in culture with CD25⁺ by itself or together with IVIg was also assessed. The presence of IVIg with Treg cells in culture significantly increased the intracellular expression of TGF- (17.7 ± 8.5% vs 29.8 ± 13%; p = 0.02), IL-10 (20.7 ± 4.7% vs 34.2 ± 5.2%; p = 0.008) and FoxP3 (20.8 ± 5.2% vs 33.7 ± 5.9%; p = 0.0006) when compared with cells cultured alone or with control human IgG. The suppressive effect of CD4⁺CD25⁺ T cells presented as the decrease of TNF- production by stimulated CD4⁺CD25^– (effector T cells) was further increased by adding IVIg to cell culture. We hereby demonstrate an additional mechanism by which IVIg could maintain self-tolerance and decrease immune-mediated inflammation.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ Address correspondence and reprint requests to Dr. Elias Toubi, Division of Clinical Immunology, Bnai-Zion Medical Centre, Technion, Haifa 31048, Israel. E-mail address: elias.toubi{at}b-zion.org.il

² Abbreviations used in this paper: ITP, idiopathic thrombocytopenic purpura; SLE, systemic lupus erythematosus; RA, rheumatoid arthritis; DC, dendritic cell.

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The JI 2007 179: 4951-4952. [Full Text]  

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