Related Experiment Video

Updated: Aug 8, 2026

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia
09:52

A Chromatin Immunoprecipitation Assay to Identify Novel NFAT2 Target Genes in Chronic Lymphocytic Leukemia

Published on: December 4, 2018

NFAT transcription factors--new players in the pathogenesis of inflammatory arthropathies?

F Pessler1, L Dai, R Q Cron

  • 1Department of Pediatrics, Division of Rheumatology, The Children's Hospital of Philadelphia, 3405 Civic Center Boulevard, Philadelphia, PA 19104, USA. pessler@email.chop.edu

Autoimmunity Reviews
|January 25, 2006
PubMed

Insights

Nuclear factor of activated T cells (NFAT) signaling is implicated in inflammatory arthropathies. Targeting NFAT may offer new therapeutic strategies for rheumatoid arthritis and related autoimmune diseases.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Inflammatory arthropathies involve significant gene expression alterations.
  • These changes stem from distinct intracellular signaling pathway activities.
  • Inducible transcription factors regulate these pathways.

Purpose of the Study:

  • To explore the role of the nuclear factor of activated T cells (NFAT) family in inflammatory arthropathies.
  • To investigate the potential of anti-NFAT therapies for autoimmune disorders.

Main Methods:

  • Analysis of gene expression changes in inflammatory arthropathies.
  • Investigation of intracellular signaling pathways and transcription factor activity.
  • Review of emerging evidence implicating NFAT in disease pathogenesis.

Main Results:

  • NFAT transcription factors are involved in immune system and tissue processes.
  • Preliminary data suggests NFAT family members play a direct role in inflammatory arthropathy development.
  • Targeting NFAT presents a potential therapeutic avenue.

Conclusions:

  • NFAT signaling is a key player in the pathogenesis of inflammatory arthropathies.
  • Anti-NFAT drug therapy could be a valuable addition to treatments for rheumatoid arthritis and other autoimmune conditions.

More Related Videos

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness08:52

Software-Assisted Quantitative Measurement of Osteoarthritic Subchondral Bone Thickness

Published on: March 18, 2022

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice07:37

An Adoptive Transfer Model of Rheumatoid Arthritis in Mice

Published on: June 6, 2025

Related Concept Videos

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...
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...
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...
Chronic Inflammation: Introduction01:12

Chronic Inflammation: Introduction

Chronic inflammation is a prolonged, dysregulated immune response that persists for weeks to years when the inciting stimulus is difficult to eradicate or when self‑antigens drive ongoing reactivity. Morphologically, it is defined by mononuclear cell infiltration, progressive tissue destruction, and concurrent attempts at healing via angiogenesis and fibrosis. Compared with acute inflammation, edema is less prominent while cellular infiltration predominates; triggers include persistent...
Inflammatory Bowel Disease II: Ulcerative Colitis01:20

Inflammatory Bowel Disease II: Ulcerative Colitis

Ulcerative colitis is a chronic inflammatory disorder of the colon characterized by continuous mucosal inflammation that typically begins in the rectum and extends proximally in a uniform pattern. Its pathogenesis involves a complex interplay of genetic predisposition, immune dysregulation, and environmental influences. These factors converge to impair the colon’s epithelial defenses and promote an exaggerated inflammatory response against luminal contents.Breakdown of the Mucosal BarrierA...
Inflammatory Bowel Disease III: Crohn's Disease01:25

Inflammatory Bowel Disease III: Crohn's Disease

Crohn’s disease is a chronic, relapsing form of inflammatory bowel disease characterized by segmental, transmural inflammation that can affect any part of the gastrointestinal tract. Its pathogenesis arises from a combination of genetic susceptibility, environmental exposures, epithelial barrier dysfunction, and immune dysregulation. Together, these factors lead to an exaggerated immune response against components of the gut microbiome.Genetic and Environmental InfluencesMultiple genetic...