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Updated: Jun 19, 2026
12:04
The bm12 Inducible Model of Systemic Lupus Erythematosus (SLE) in C57BL/6 Mice
Published on: November 1, 2015
Nph, DC and chromatin-mediated pathogenesis in systemic lupus erythematosus
Dennis Lindau1, Patrice Decker
1Department of Immunology, Institute for Cell Biology, University of Tübingen, Tübingen, Germany.
Autoimmunity
|October 9, 2009
Summary
Nucleosomes are key lupus autoantigens that trigger inflammation by activating immune cells and the complement system. Understanding their signaling pathways is crucial for lupus pathogenesis in predisposed individuals.
Area of Science:
- Immunology
- Autoimmunity
- Molecular Biology
Background:
- Nucleosomes (Nuc) are significant autoantigens in lupus.
- Nuc activate immune cells and the complement system, leading to inflammation.
- Elevated Nuc concentrations may break peripheral tolerance in genetically susceptible individuals.
Purpose of the Study:
- To elucidate the signaling pathways involved in nucleosome-mediated immune cell activation.
- To understand the role of Tir8/Sigirr in the response to nucleosome-containing immune complexes.
Main Methods:
- Investigated immune cell activation upon exposure to nucleosomes.
- Analyzed the role of Tir8/Sigirr deficiency in nucleosome-induced responses.
Main Results:
- Nucleosomes activate immune cells and the complement system, contributing to inflammation.
- Tir8/Sigirr deficiency was observed to enhance cell activation when exposed to Nuc-containing immune complexes.
Conclusions:
- Nucleosomes are potent immune stimulants in lupus.
- Further research into nucleosome signaling pathways, particularly involving Tir8/Sigirr, is warranted to understand lupus pathogenesis and tolerance breakdown.
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