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Screening Bioactive Nanoparticles in Phagocytic Immune Cells for Inhibitors of Toll-like Receptor Signaling

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Published on: July 26, 2017

[Functional Study of TNFR2 Signaling and Drug Discovery Using a Protein Engineering Approach].

Shin-Ichi Tsunoda¹

¹Faculty of Pharmaceutical Sciences, Kobe Gakuin University.

Yakugaku Zasshi : Journal of the Pharmaceutical Society of Japan

|November 30, 2022

Summary

This summary is machine-generated.

Tumor necrosis factor-α (TNF) receptor 2 (TNFR2) promotes regulatory T cell (Treg) activation and proliferation. This study identified TNFR2

Keywords:

mutant cytokine phage display library regulatory T cell type II tumor necrosis factor-α receptor

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Published on: December 1, 2020

Area of Science:

Immunology and Molecular Biology
Cytokine Receptor Signaling

Context:

Tumor necrosis factor-α (TNF) is a key inflammatory cytokine, with TNFR1 primarily implicated in inflammation.
Emerging evidence suggests TNFR2 possesses anti-inflammatory functions, but its mechanisms remain unclear.

Purpose:

To elucidate the anti-inflammatory mechanisms of TNFR2 and its other biological functions.
To utilize protein engineering to generate functional mutant cytokines for studying TNFR2.

Summary:

TNFR2 is expressed on regulatory T cells (Tregs), promoting their proliferation and activation.
The crystal structure of the TNF/TNFR2 complex suggests signal initiation via membrane cluster formation.
Aminopeptidase P3 (APP3/XPNPEP3) was identified as a novel intracellular adaptor protein for TNFR2, essential for JNK phosphorylation.

Impact:

Provides critical insights into immune regulation mechanisms involving TNFR2 and Tregs.
Aids in identifying novel immunomodulatory drugs targeting the TNFR2 signaling pathway.