Research ArticleLupus

NADPH Oxidase Inhibits the Pathogenesis of Systemic Lupus Erythematosus

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Science Translational Medicine  24 Oct 2012:
Vol. 4, Issue 157, pp. 157ra141
DOI: 10.1126/scitranslmed.3004801

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Casting a Wider NET for Lupus Autoantigen

Systemic lupus erythematosus (SLE) is an autoimmune disease in which the body’s immune system attacks its own healthy tissue. Patients with SLE may have inflammation in a broad range of organs, including skin, joints, kidneys, and brain. There is no cure for SLE, and the source of the underlying antigens targeted by the immune system—autoantigens—remains unknown. Recent studies have suggested that neutrophil extracellular traps (NETs), which release nucleic acids outside the cell, are one potential source for autoantigen in SLE. Now, Campbell et al. test the contribution of NETs in vivo in a mouse model of SLE.

NET release relies on the expression of NADPH oxidase (Nox2). If NETs were required for SLE pathology, mice prone to lupus that lack Nox2 should not develop disease. Instead, the authors found that such mice actually had exacerbated lupus-related symptoms. Indeed, failure of Nox2-mediated cell death may stimulate lupus development. These results are consistent with studies that link Nox2 deficiency to lupus symptoms in humans. Although the complete mechanism leading to lupus exacerbation must still be elucidated, this study suggests that SLE is not nothing but NET.

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