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Here we report that granulocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase crucially contributes to tissue injury in experimental models of the antibody\u2010mediated autoimmune disease epidermolysis bullosa acquisita. Neutrophil cytosolic factor 1\u2010deficient mice lacking functional NADPH oxidase were resistant to skin blistering by the passive transfer of antibodies against type VII collagen. Pharmacological inhibition or deficiency of human NADPH oxidase abolished dermal\u2010epidermal separation caused by autoantibodies and granulocytes <jats:italic>ex vivo<\/jats:italic>. In addition, recruitment of granulocytes into the skin was required for tissue injury, as demonstrated by the resistance to experimental blistering of wild\u2010type mice depleted of neutrophils and of CD18\u2010deficient mice. Transfer of neutrophil cytosolic factor 1\u2010sufficient granulocytes into neutrophil cytosolic factor 1\u2010deficient mice demonstrated that granulocytes provide the NADPH oxidase required for tissue damage. Our findings identify granulocyte\u2010derived NADPH oxidase as a key molecular effector engaged by pathogenic autoantibodies and provide relevant targets for prevention of tissue damage in granulocyte\u2010mediated autoimmune diseases. Copyright \u00a9 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley &amp; Sons, Ltd.<\/jats:p>","DOI":"10.1002\/path.2157","type":"journal-article","created":{"date-parts":[[2007,3,23]],"date-time":"2007-03-23T08:06:44Z","timestamp":1174637204000},"page":"56-65","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":141,"title":["NADPH oxidase is required for neutrophil\u2010dependent autoantibody\u2010induced tissue 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