Newer insights into the aetiology and pathogenesis of myeloperoxidase associated autoimmunity.

Jpn J Infect Dis

Vth Medical Clinic, University Hospital Mannheim, Heidelberg University, Mannheim, Germany.

Published: October 2004

AI Article Synopsis

  • Recent advancements have clarified the causes and development of ANCA-associated vasculitides, particularly MPO autoimmunity.
  • The review highlights genetic and environmental risk factors, and the roles of T-cells, B-cells, and ANCA in disease progression.
  • Evidence shows that reactivation of certain gene expressions and anti-idiotypic antibodies against PR3 may play significant roles in the disease's pathogenesis.

Article Abstract

In recent years there have been substantial developments in the understanding of the aetiology and pathogenesis of ANCA-associated vasculitides, including myeloperoxidase (MPO) associated autoimmunity. This review will describe genetic and environmental factors that may increase the risk for the disease and will summarise findings demonstrating that T-cells, B-cells and ANCA themselves are of pathogenetic significance. Leukocyte gene expression profiles indicate that the reactivation of granule protein genes contributes to the pathogenesis of AASV. Finally, data derived from closely related autoantibodies against proteinase 3 (PR3) suggest anti-idiotypic antibodies induced by antisense transcripts as potential pathological agents.

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