Breaking immunological tolerance in systemic lupus erythematosus
SourceFrontiers in Immunology, 5, (2014), article 164
Article / Letter to editor
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Frontiers in Immunology
SubjectRadboudumc 11: Renal disorders RIMLS: Radboud Institute for Molecular Life Sciences
Systemic lupus erythematosus (SLE) is a fairly heterogeneous autoimmune disease of unknown etiology that mainly affects women in the childbearing age. SLE is a prototype type III hypersensitivity reaction in which immune complex depositions cause inflammation and tissue damage in multiple organs. Two distinct cell death pathways, apoptosis and NETosis, gained a great deal of interest among scientists, since both processes seem to be deregulated in SLE. There is growing evidence that histone modifications induced by these cell death pathways exert a central role in the induction of autoimmunity. In the current review, we discuss how abnormalities in apoptosis, NETosis, and histone modifications may lead to a break of immunological tolerance in SLE.
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