Document Detail

Pathogenesis of antineutrophil cytoplasmic autoantibody-associated small-vessel vasculitis.
MedLine Citation:
PMID:  23347350     Owner:  NLM     Status:  In-Data-Review    
Clinical, in vitro, and experimental animal observations indicate that antineutrophil cytoplasmic autoantibodies (ANCA) are pathogenic. The genesis of the ANCA autoimmune response is a multifactorial process that includes genetic predisposition, environmental adjuvant factors, an initiating antigen, and failure of T cell regulation. ANCA activate primed neutrophils (and monocytes) by binding to certain antigens expressed on the surface of neutrophils in specific inflammatory microenvironments. ANCA-activated neutrophils activate the alternative complement pathway, establishing an inflammatory amplification loop. The acute injury elicits an innate inflammatory response that recruits monocytes and T lymphocytes, which replace the neutrophils that have undergone karyorrhexis during acute inflammation. Extravascular granulomatous inflammation may be initiated by ANCA-induced activation of extravascular neutrophils, causing tissue necrosis and fibrin formation, which would elicit an influx of monocytes that transform into macrophages and multinucleated giant cells. Over time, the neutrophil-rich acute necrotizing lesions cause the accumulation of more lymphocytes, monocytes, and macrophages and produce typical granulomatous inflammation.
J Charles Jennette; Ronald J Falk; Peiqi Hu; Hong Xiao
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Annual review of pathology     Volume:  8     ISSN:  1553-4014     ISO Abbreviation:  Annu Rev Pathol     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2013-01-25     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101275111     Medline TA:  Annu Rev Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  139-60     Citation Subset:  IM    
Department of Pathology and Laboratory Medicine, and UNC Kidney Center, University of North Carolina, Chapel Hill, North Carolina 27599; email: , , ,
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