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Related Experiment Video

Updated: May 29, 2026

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

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Published on: June 14, 2018

Interferon alpha as a primary pathogenic factor in human lupus.

Timothy B Niewold¹

¹Section of Rheumatology, Gwen Knapp Center for Lupus and Immunology Research, University of Chicago, Chicago, Illinois 60637, USA. tniewold@medicine.bsd.uchicago.edu

Journal of Interferon & Cytokine Research : the Official Journal of the International Society for Interferon and Cytokine Research

|September 20, 2011

Summary

This summary is machine-generated.

Interferon alpha (IFN-α) plays a key role in initiating systemic lupus erythematosus (SLE). Genetic factors and IFN-α treatments can increase SLE risk, suggesting a link between viral defense and autoimmunity.

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Area of Science:

Immunology
Genetics
Autoimmunity

Background:

Interferon alpha (IFN-α) is crucial in viral immunity, bridging innate and adaptive immune responses.
Its role in autoimmunity, particularly systemic lupus erythematosus (SLE), is increasingly recognized.

Purpose of the Study:

To review evidence supporting the role of IFN-α in the initiation of human SLE.
To explore genetic and environmental factors contributing to IFN-α dysregulation in SLE.

Main Methods:

Review of existing literature and clinical data.
Analysis of genetic association studies and family-based studies.
Examination of cases of de novo SLE following IFN-α treatment.

Main Results:

IFN-α treatment can trigger de novo SLE, which often resolves upon withdrawal.
Elevated serum IFN-α levels are observed within SLE families, indicating a heritable risk.
Gain-of-function genetic variants in the IFN-α pathway are associated with increased SLE susceptibility.

Conclusions:

Genetically determined elevations in endogenous IFN-α predispose individuals to human SLE.
The heightened IFN-α activity may represent a trade-off for enhanced viral defense.
Understanding the IFN-α pathway is critical for SLE pathogenesis and potential therapeutic strategies.