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NF-κB-dependent Signaling Pathway

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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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Related Experiment Video

Updated: May 26, 2026

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Screening Assays to Characterize Novel Endothelial Regulators Involved in the Inflammatory Response

Published on: September 15, 2017

TNF superfamily in inflammatory disease: translating basic insights.

Michael Croft¹, Wei Duan, Heonsik Choi

¹La Jolla Institute for Allergy and Immunology, Division of Immune Regulation, 9420 Athena Circle, La Jolla, CA 92037, USA. mick@liai.org

Trends in Immunology

|December 16, 2011

Summary

Tumor necrosis factor (TNF) and its receptor superfamily (TNFSF/TNFRSF) proteins regulate immune cells and are implicated in autoimmune diseases. Targeting these pathways shows promise for treating inflammatory conditions.

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Area of Science:

Immunology
Molecular Biology
Cell Biology

Background:

The tumor necrosis factor (TNF) and TNF receptor superfamilies (TNFSF and TNFRSF) comprise around 50 proteins involved in cellular function.
These molecules primarily interact with immune cells, influencing differentiation, survival, and inflammatory mediator production.

Purpose of the Study:

To review current research on the therapeutic potential of TNFSF and TNFRSF molecules in autoimmune and inflammatory diseases.

Main Methods:

Literature review of recent data on TNFSF and TNFRSF signaling pathways.
Analysis of genetic associations between TNFSF/TNFRSF polymorphisms and disease susceptibility.

Main Results:

TNFSF ligand-receptor signaling is active in inflammatory and autoimmune conditions.
Genetic variations in TNFSF and TNFRSF are linked to increased susceptibility to certain diseases.

Conclusions:

The TNFSF and TNFRSF represent promising therapeutic targets for autoimmune and inflammatory diseases.