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FOXP3 biochemistry will lead to novel drug approaches for vaccines and diseases that lack suppressor T cells

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The Immune Synapse as a Novel Target for Therapy

Abstract

FOXP3 is a forkhead family transcription factor, which acts as a master regulator in the development of natural regulatory T cells (Tregs) and their function in the control of self tolerance [1]. Natural Tregs, which represent about 5–10% of total CD4+ T cells, develop in the thymus and have a middle-high TCR-binding affinity. Tregs function as suppressors of multiple immune cells including CD4 effector T cells, CD8 cytotoxic T cells, B cells, NK cells, and dendritic cells in vivo [2]. Although the molecular mechanism by which Tregs suppress these multiple immune cells in a cell-cell contact-dependent manner is largely unknown [3], recent experimental evidence supports the notion that the level and duration of FOXP3 expression is essential to Treg-mediated dominant suppression [4, 5]. A complete understanding of the biochemistry of FOXP3 activity in Tregs will have therapeutic implications for transplantation, allergy, autoimmune disease, inflammatory disease, vaccine development and cancer [6].

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Li, B. et al. (2008). FOXP3 biochemistry will lead to novel drug approaches for vaccines and diseases that lack suppressor T cells. In: Graca, L. (eds) The Immune Synapse as a Novel Target for Therapy. Progress in Inflammation Research. Birkhäuser Basel. https://doi.org/10.1007/978-3-7643-8296-4_10

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