Linked Life Data

17380558

Source:http://linkedlifedata.com/resource/pubmed/id/17380558

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2007-5-24
pubmed:abstractText
The contribution of phagocyte-derived reactive oxygen species to tissue injury in autoimmune inflammatory diseases is unclear. Here we report that granulocyte nicotinamide adenine dinucleotide phosphate (NADPH) oxidase crucially contributes to tissue injury in experimental models of the antibody-mediated autoimmune disease epidermolysis bullosa acquisita. Neutrophil cytosolic factor 1-deficient 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-epidermal separation caused by autoantibodies and granulocytes ex vivo. In addition, recruitment of granulocytes into the skin was required for tissue injury, as demonstrated by the resistance to experimental blistering of wild-type mice depleted of neutrophils and of CD18-deficient mice. Transfer of neutrophil cytosolic factor 1-sufficient granulocytes into neutrophil cytosolic factor 1-deficient mice demonstrated that granulocytes provide the NADPH oxidase required for tissue damage. Our findings identify granulocyte-derived NADPH oxidase as a key molecular effector engaged by pathogenic autoantibodies and provide relevant targets for prevention of tissue damage in granulocyte-mediated autoimmune diseases.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-3417
pubmed:author
pubmed:copyrightInfo
Copyright (c) 2007 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
pubmed:issnType
Print
pubmed:volume
212
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
56-65
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
NADPH oxidase is required for neutrophil-dependent autoantibody-induced tissue damage.
pubmed:affiliation
Department of Dermatology, University of Lübeck, Lübeck, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't