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The transcription factor NF-κB was discovered in 1986 in the lab of Nobel laureate Professor David Baltimore, for its interaction with the immunoglobulin light chain enhancer in B-cells. After more than three decades of study, it is now evident that NF-κB regulates the expression of over 100 genes. Most of these genes play an essential role in the innate and adaptive immune responses as well as the inflammatory responses of animals.
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Updated: Jun 29, 2025

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TNFR2 signalling in inflammatory diseases.

Richard O Williams1, Felix Il Clanchy1, Yi-Shu Huang1

  • 1Kennedy Institute of Rheumatology, University of Oxford, Roosevelt Drive, Oxford, OX3 7FY, UK.

Best Practice & Research. Clinical Rheumatology
|March 27, 2024
PubMed
Summary
This summary is machine-generated.

Targeting tumor necrosis factor (TNF) receptors selectively offers new therapeutic strategies. Inhibiting TNFR1 may treat autoimmune diseases, while TNFR2 agonists could aid cancer therapy.

Keywords:
AutoimmunityInflammationRheumatoid arthritisTNFTNF receptors

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Area of Science:

  • Immunology
  • Molecular Biology
  • Pharmacology

Background:

  • Tumor necrosis factor (TNF) signals through two receptors: TNFR1 and TNFR2.
  • TNFR1 mediates pro-inflammatory effects, while TNFR2 is involved in immune homeostasis and tissue healing, but also tumor progression.
  • Current anti-TNF biologics lack selectivity, inhibiting both TNFR1 and TNFR2.

Purpose of the Study:

  • To explore the therapeutic potential of selective TNF receptor inhibitors.
  • To investigate TNFR1 inhibition for autoimmune diseases and TNFR2 inhibition for cancer.
  • To evaluate TNFR2 agonists as a potential therapeutic approach.

Main Methods:

  • The study hypothesizes the selective inhibition of TNFR1 in autoimmune diseases.
  • It explores the development of TNFR1-selective inhibitors and TNFR2-specific agonists.
  • The research discusses the validation of these concepts for novel therapeutic strategies.

Main Results:

  • Selective TNFR1 inhibition is hypothesized to alleviate inflammation and promote homeostasis in autoimmune diseases.
  • TNFR2 signaling is proposed to proceed unimpeded with TNFR1 inhibition, aiding homeostasis.
  • TNFR2-specific agonists are being explored for monotherapy or combination treatment.

Conclusions:

  • Selective inhibition of TNF receptors presents a promising therapeutic avenue.
  • TNFR1 antagonists could treat autoimmune conditions by reducing inflammation.
  • TNFR2 agonists may offer new strategies for cancer treatment.