CD163 and systemic lupus erythematosus: CD163 has been suggested as a urinary biomarker of activity in LN.18 The presence of type I IFN signalling has been associated with mitochondrial abnormalities, leading to mitochondrial insufficiency and increased cell death as a regulatory mechanism in persistent type I IFN response.21 However, it has been demonstrated in animal models that altered metabolic dysfunction is a reversible change in lupus affected tissues, not driven by type I IFN exposure, and correct modulation can be restored after immunosuppression in animal models.28