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Related Experiment Video

Updated: Jun 10, 2026

Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α

Development and Validation of an Ultrasensitive Single Molecule Array Digital Enzyme-linked Immunosorbent Assay for Human Interferon-α

Published on: June 14, 2018

Interferon alpha in systemic lupus erythematosus.

Timothy B Niewold¹, Daniel N Clark, Rafah Salloum

¹Section of Rheumatology and Gwen Knapp Center for Lupus and Immunology Research, The University of Chicago, Chicago, IL 60637, USA.

Journal of Biomedicine & Biotechnology

|July 24, 2010

Summary

This summary is machine-generated.

Interferon alpha (IFN-α) plays a key role in lupus development and symptoms. Elevated IFN-α levels in lupus patients link genetic risks to disease effects, suggesting it as a therapeutic target.

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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice

Published on: November 1, 2015

Area of Science:

Immunology
Rheumatology
Genetics

Background:

Interferon alpha (IFN-α) is a pleiotropic cytokine crucial for antiviral responses and immune activation.
Elevated serum IFN-α levels and interferon response gene expression are prevalent in systemic lupus erythematosus (SLE) patients.
Heightened IFN-α can disrupt immune regulation and is implicated in lupus pathogenesis.

Purpose of the Study:

To provide a comprehensive overview of interferon alpha's role in lupus.
To explore the cellular, genetic, and clinical aspects of IFN-α in SLE.
To highlight IFN-α as a potential therapeutic target in lupus.

Main Methods:

Literature review and synthesis of existing research on interferon alpha and lupus.
Analysis of genetic associations with interferon production and signaling pathways in SLE.
Correlation of cellular and clinical manifestations with elevated IFN-α levels.

Main Results:

Interferon alpha is intricately involved in lupus etiology and pathogenesis.
Autoantibodies in lupus can stimulate IFN-α production, creating a feedback loop.
Genetic factors influencing interferon pathways are linked to SLE risk.
Excess IFN-α contributes to both cellular and clinical features of lupus.

Conclusions:

Interferon alpha acts as a critical link between genetic predisposition and phenotypic expression in lupus.
The cytokine significantly influences the clinical presentation of SLE.
Interferon alpha represents a promising therapeutic target for managing lupus.