Related Experiment Video

Updated: Aug 13, 2026

Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes
11:52

Differentiation of Functional Osteoclasts from Human Peripheral Blood CD14+ Monocytes

Published on: January 27, 2023

Tumor necrosis factor ligand-receptor superfamily and arthritis

Hui-Chen Hsu1, Yalei Wu, John D Mountz

  • 1Department of Medicine, Division of Clinical Immunology and Rheumatology, University of Alabama at Birmingham, Birmingham, AL 35294, USA.

Current Directions in Autoimmunity
|January 6, 2006
PubMed

Insights

Defects in apoptosis regulation involving TNF ligand-receptor superfamily (TNFRsF) molecules contribute to rheumatoid arthritis (RA). Understanding these pathways is key to developing gene therapies for RA prevention.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Rheumatoid arthritis (RA) pathogenesis involves complex dysregulation of apoptosis.
  • TNF ligand-receptor superfamily (TNFRsF) molecules play a critical role in immune cell function and apoptosis.
  • Aberrant apoptosis in lymphocytes and synovial fibroblasts contributes to RA development and joint damage.

Purpose of the Study:

  • To review the regulation of TNFRsF molecules in RA.
  • To elucidate the pathogenic roles of TNFRsF in RA.
  • To identify potential therapeutic targets for modulating apoptosis in RA.

Main Methods:

  • Literature review of studies on apoptosis and RA.
  • Analysis of TNFRsF regulation and function.
  • Examination of molecular and cellular mechanisms in RA pathogenesis.

Main Results:

  • Defects in apoptosis at various levels and in different cell types can lead to RA.
  • Dysregulated apoptosis contributes to T cell and synovial hyperproliferation, defective or excessive apoptosis, and bone erosion.
  • TNFRsF molecules are implicated in the induction or prevention of RA.

Conclusions:

  • Understanding TNFRsF regulation is crucial for RA treatment.
  • Targeting specific cells and molecules involved in apoptosis modulation offers a promising strategy for RA prevention.
  • Gene therapy approaches targeting apoptosis pathways may prevent RA development.

Related Concept Videos

T Cell Types and Functions01:24

T Cell Types and Functions

When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF01:24

Drugs for Treatment of Crohn's Disease in IBD Using Biologic Agents: Anti-TNF

Tumor Necrosis Factor (TNF), a proinflammatory cytokine, contributes significantly to the inflammation seen in Crohn's disease. It exists as soluble TNF and membrane-bound TNF, with actions mediated through TNF receptors (TNFR). TNFR activation leads to the release of proinflammatory cytokines, T-cell activation, collagen production, and leukocyte migration, all contributing to inflammation in Crohn's disease. Anti-TNF monoclonal antibodies, namely infliximab (Remicade), adalimumab (Humira),...
Enzyme-linked Receptors01:00

Enzyme-linked Receptors

Enzyme-linked receptors are proteins that act as both receptor and enzyme, activating multiple intracellular signals. This is a large group of receptors that include the receptor tyrosine kinase (RTK) family. Many growth factors and hormones bind to and activate the RTKs.
Neurotrophin (NT) receptors are a family of RTKs, including trkA, trkB, and trkC (tropomyosin-related kinase) receptors. TrkA is specific for nerve growth factor (NGF), neurotrophin-6, and neurotrophin-7. TrkB binds...
The JAK-STAT Signaling Pathway01:20

The JAK-STAT Signaling Pathway

Several cytokine receptors have tightly bound Janus kinase or JAK proteins attached at their cytosolic tail. Small signaling molecules such as cytokines, growth hormones, or prolactins bind to the cytokine receptors and initiate their dimerization. The dimerization brings the cytosolic JAKs together that trans-phosphorylate and activates each other. The activated JAKs now phosphorylate cytosolic tails of the cytokine receptors, which serve as binding sites for adaptor proteins such as  SH2...
NF-κB-dependent Signaling Pathway02:26

NF-κB-dependent Signaling Pathway

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.
NF-κB-dependent Signaling Mechanism
The heterodimer of NF-κB...
Transducer Mechanism: Enzyme-Linked Receptors01:27

Transducer Mechanism: Enzyme-Linked Receptors

Enzyme-linked receptors are cell-surface receptors acting as an enzyme or associating with an enzyme intracellularly. They make excellent drug targets. Drugs can bind to the extracellular ligand-binding domain or directly affect their enzymatic domain and alter their activity.
Major types that are helpful drug targets include: