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Subproject 7

Pathogenetic mechanisms in autoimmunity induced by deregulated zytosolic nucleic-acid recognition

Defects of the intracellular nucleases Trex1 and RNase H2 as well as mutations of the SAMHD1 gene cause a spontaneous inflammatory disease, Aicardi-Goutieres Syndrome (AGS). An uncontrolled, chronic response of the type I interferon system seems to be essential in the pathogenesis of this condition. Deregulated release of type I interferon is also a prominent feature of systemic lupus erythematosus (SLE). Intriguingly, AGS also shows lupus like symtoms, and a fraction of SLE patients carry mutations in the TREX1 gene, indicating that the two diseases are pathogenetically related. Trex1-deficient mice develop interferon-dependent autoimmune myocarditis, while no animal models exist for defects of the other AGS-associated genes. We are generating conventional and cell type-specific knock out mouse strains for the genes TREX1, RNASEH2A-C and SAMHD1 in order to study the pathogenesis of the interferonopathies ensuing from defects of these genes in humans.



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Project leader:

Axel Roers

Prof. Dr. med. Axel Roers

Institut für Immunologie
Tel.: 0351-458 6500

Sekretariat: Julia Seifert
Tel.: 0351-458 6505
Email: julia.seifert@