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Abstract
Nucleosomes (Nuc) are key lupus autoantigen and have been shown to activate several types of immune cells as well as the complement system, resulting in inflammation. The elevated concentrations and the immunostimulatory capacities of circulating Nuc may favour the break of peripheral tolerance in genetically predisposed individuals. Nevertheless, in most cases the signalling pathways involved are not elucidated yet, although Tir8/Sigirr deficiency has been recently shown to enhance cell activation upon exposure to Nuc-containing immune complexes [1].