Related Experiment Video
Updated: Feb 19, 2026

08:26
Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α
Published on: June 14, 2018
12.6K
Targeting interferons and their pathways in systemic lupus erythematosus
François Chasset1, Laurent Arnaud2
1AP-HP, Service de Dermatologie et d'Allergologie, Hôpital Tenon, F-75020, Paris, France.
Autoimmunity Reviews
|November 8, 2017
Summary
Interferons (IFNs) are key in Systemic Lupus Erythematosus (SLE) pathogenesis. Targeting IFN pathways, including novel antibody and small molecule inhibitors, shows promise for developing new SLE therapeutics.
Area of Science:
- Immunology
- Rheumatology
Background:
- Interferons (IFNs), particularly IFN-α, are central mediators in Systemic Lupus Erythematosus (SLE) pathogenesis.
- Advances in understanding innate immunity highlight the role of IFNs in SLE.
Purpose of the Study:
- To review current and emerging therapeutic strategies targeting interferon pathways in SLE.
- To discuss novel drug research focused on blocking IFNs and their downstream signaling.
Main Methods:
- Review of clinical trials assessing anti-IFN-α antibodies, anti-type I interferon receptor antibodies, and other IFN-blocking agents.
- Investigation of alternative strategies targeting plasmacytoid dendritic cells (pDCs), Toll-Like Receptors (TLRs), and downstream signaling molecules (MYD88, Syk, JAKs, IRAK4, TYK2).
Main Results:
- Several interferon-blocking strategies have been evaluated in clinical trials.
- Targeting pDCs, TLRs, and downstream kinases (JAKs, TYK2) are under active investigation, with JAK inhibitors reaching Phase 2 studies.
Conclusions:
- Targeting IFNs and their pathways represents a significant development in novel drug research for SLE.
- Personalized functional characterization of IFN pathways may guide future tailored therapeutic strategies for SLE patients.
Related Concept Videos
The JAK-STAT Signaling Pathway
13.2K
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...
13.2K
T Cell Types and Functions
2.7K
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...
Th1 cells stimulate dendritic cells to express necessary co-stimulatory molecules on their surfaces for...
2.7K
Immune Response Against Viral Pathogens
2.2K
The immune system's response to viral infections is a complex and coordinated process involving natural killer (NK) cells, T cell-mediated responses, and antibody-mediated responses.
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
NK Cells
NK cells are a crucial part of our innate immune system, acting as the first line of defense against viral infections. These cells can recognize and kill infected cells without prior exposure to the virus, effectively slowing down the spread of infection. Additionally, NK cells produce proinflammatory...
2.2K

