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Lupus nephritis is a frequent complication of systemic lupus erythematosus. Multiple pathological mechanisms attribute to the pathogenesis of lupus nephritis. These mechanisms can be grossly divided into two groups, extrarenal or intrarenal pathways. A variety of genetic variants break immune tolerance to nuclear autoantigens, as evident from the existence of antinuclear antibodies. Furthermore, molecular mimicry of endogenous nucleic acids activating Toll-like receptors trigger antiviral immunity. In this review, we discuss the molecular pathomechanisms of lupus nephritis.
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Devarapu et al. (2016) studied this question.
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