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The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Vicious circle: systemic autoreactivity in Ro52/TRIM21-deficient mice
Silvia Bolland1, Adolfo Garcia-Sastre
1Laboratory of Immunogenetics, National Institute of Allergy and Infectious Disease, National Institutes of Health, Rockville MD 20852, USA. SBolland@niaid.nih.gov
The Journal of Experimental Medicine
|July 29, 2009
Summary
Excessive interferon pathways can cause autoimmune diseases. Ro autoantigens, like Ro52/Trim21, prevent autoimmunity by inhibiting interferon regulatory factors (IRFs).
Area of Science:
- Immunology
- Autoimmunity
- Innate Immune Responses
Background:
- Dysregulated innate immune responses, especially overactive interferon (IFN) pathways, are linked to autoimmune diseases.
- Autoimmunity often targets IFN-inducible genes, including Ro autoantigens, which regulate interferon regulatory factors (IRFs).
Purpose of the Study:
- To validate the role of Ro autoantigens in preventing autoimmunity.
- To investigate the mechanisms underlying injury-induced systemic autoimmune disease.
Main Methods:
- Investigated the role of Ro52/Trim21 in a mouse model of autoimmune disease.
- Analyzed the involvement of the IL-23-Th17 pathway in disease exacerbation.
Main Results:
- Absence of Ro52/Trim21 exacerbated injury-induced systemic autoimmune disease.
- The IL-23-Th17 pathway was identified as a key driver of exacerbated autoimmune disease in the absence of Ro52/Trim21.
Conclusions:
- Ro autoantigens, specifically Ro52/Trim21, play a crucial role in preventing autoimmunity.
- The IL-23-Th17 pathway is a critical mediator in the development of autoimmune pathology when Ro52/Trim21 is absent.
