Overexpression of SATB1 Gene Inhibits the Immunosuppressive Function of Regulatory T Cells in Chronic Hepatitis B

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Abstract

Abstract.

Special AT-rich sequence-binding protein 1 (SATB1) is a class of nuclear matrix binding protein expressed by T cells and plays an important role in regulatory T cells (Tregs) mediated immune regulation. The immunosuppressive function of Tregs in chronic hepatitis B (CHB) being inhibited by SATB1 has been shown in our previous studies. The objective of this study was to learn the impact of SATB1 on the cellular immune function of CHB. SATB1 isolated from human peripheral blood mononuclear cells (PBMCs) was used as a template of PCR and its product was connected to vector PLV-EF1α-EGFP-N. Reconstructed vector PLV-EF1α-SATB1/EGFP was used to create highly infectious virions and then transduced to Tregs isolated from the CHB patients. Cytokine secreted by Tregs with and without SATB1 overexpression were determined. The results showed that there was a significant increase of Th1 (IFN-γ) and Th2 (IL-4 and IL-5) cytokines following SATB1 overexpression in CHB derived Tregs. It means that overexpression of SATB1 can promote the conversion from Tregs to effector T cells (Teffs) that lose suppressive function and stimulate the secretion of effective cytokines. These data provide the basis for further research on the mechanism of SATB1 in regulating specific immune response of CHB patients.

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