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. It has been shown previously that proteinase 3 (PR3), a neutrophil intracellular protease that is the main antigen of antineutrophil cytoplasm (ANCA) autoantibodies, is present on the plasma membrane of a subset of freshly isolated neutrophils. This study shows that the size of this subset of membrane PR3-positive (mPR3 + ) neutrophils is a stable feature of a given individual, most likely genetically controlled. It ranges from 0 to 100% of neutrophils and allows us to define a new polymorphism in the healthy population, with three discrete phenotypes corresponding respectively to less than 20% mPR3 +  neutrophils (mPR3 low ) or to a mean percentage of 47% (mPR3 intermediate ) and 71.5% (mPR3 high ) mPR3 +  neutrophils. The frequency of the mPR3 high  phenotype was significantly increased in patients with ANCA-associated vasculitis (85%  versus  55% in healthy subjects). The percentage of mPR3 +  neutrophils was not affected by disease activity, relapses, or therapy, and did not reflect  in vivo  cell activation. In addition, mPR3 +  phenotypes were normally distributed in cystic fibrosis patients, indicating that infection and/or inflammation  per se  do not lead to a high percentage of mPR3 +  neutrophils. The frequency of the mPR3 high  phenotype was not related to anti-PR3 autoimmunization, since it was increased in vasculitic patients regardless of the ANCA specificity (anti-PR3, anti-myeloperoxidase, or unknown). Interestingly, the frequency of the mPR3 high  phenotype was also increased in patients with rheumatoid arthritis. It was normal in type I-diabetes, a T cell-dependent autoimmune disease. It is proposed here that a high proportion of membrane PR3-positive neutrophils could favor the occurrence or the progression of chronic inflammatory diseases.

A Large Subset of Neutrophils Expressing Membrane Proteinase 3 Is a Risk Factor for Vasculitis and Rheumatoid Arthritis