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In Vitro and In Vivo Assessment of T, B and Myeloid Cells Suppressive Activity and Humoral Responses from Transplant Recipients
Published on: August 12, 2017
Intravenous immunoglobulin therapy affects T regulatory cells by increasing their suppressive function
Aharon Kessel1, Hana Ammuri, Regina Peri
1Division of Clinical Immunology, Bnai-Zion Medical Centre, Rappaport Faculty of Medicine, Technion, Haifa, Israel.
Intravenous immunoglobulin therapy (IVIg) boosts regulatory T cells (Treg), increasing TGF-beta, IL-10, and FoxP3 expression. This enhances Treg suppressive function, offering a new mechanism for IVIg in treating autoimmune diseases.
Area of Science:
- Immunology
- Cell Biology
- Autoimmune Disease Research
Background:
- Intravenous immunoglobulin therapy (IVIg) is a recognized treatment for autoimmune diseases.
- The precise mechanisms by which IVIg exerts its therapeutic effects are not fully elucidated.
- Regulatory T cells (Tregs) play a crucial role in maintaining immune tolerance.
Purpose of the Study:
- To investigate the in vitro effect of IVIg on the expression of key regulatory molecules (TGF-beta, IL-10, FoxP3) in T regulatory cells.
- To determine if IVIg enhances the suppressive capacity of Treg cells.
- To explore a potential novel mechanism of action for IVIg in immune-mediated conditions.
Main Methods:
- Human CD4(+) T cells from healthy donors were cultured with or without IVIg or control IgG for 16, 24, and 36 hours.
- Flow cytometry (FACS) was used to analyze intracellular expression of TGF-beta, IL-10, and FoxP3 within CD4(+)CD25(high) Treg cells.
- Tumor Necrosis Factor-alpha (TNF-alpha) production by stimulated effector T cells was measured in co-cultures with or without Treg cells and IVIg.
Main Results:
- IVIg significantly increased intracellular TGF-beta, IL-10, and FoxP3 expression in Treg cells compared to control IgG or no treatment (p < 0.05 for all).
- The presence of IVIg augmented the suppressive function of Treg cells, evidenced by a greater reduction in TNF-alpha production by effector T cells.
- These findings suggest IVIg directly impacts Treg cell function and molecular expression.
Conclusions:
- IVIg enhances the expression of TGF-beta, IL-10, and FoxP3 in human Treg cells in vitro.
- IVIg potentiates the suppressive activity of Treg cells, contributing to immune regulation.
- This study reveals an additional mechanism for IVIg's therapeutic efficacy in maintaining self-tolerance and reducing immune-mediated inflammation.
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