How anti-neutrophil cytoplasmic autoantibodies activate neutrophils

被引：89

作者：

Kettritz, R. ^{[1
,2
,3
]}

机构：

[1] Univ Med Berlin, Nephrol & Internist Intens Med Charite Virchow Kl, D-13125 Berlin, Germany

[2] Charite Med Fac, Expt Clin Res Ctr, Berlin, Germany

[3] Max Delbruck Ctr Mol Med, Berlin, Germany

来源：

CLINICAL AND EXPERIMENTAL IMMUNOLOGY | 2012年 / 169卷 / 03期

关键词：

ANCA; neutrophils; pathogenesis; signal transduction; vasculitis; MEMBRANE PROTEINASE-3 EXPRESSION; ANCA-ASSOCIATED VASCULITIS; HUMAN POLYMORPHONUCLEAR LEUKOCYTES; TUMOR-NECROSIS-FACTOR; FC-GAMMA-RIIIB; SYSTEMIC VASCULITIS; CRESCENTIC GLOMERULONEPHRITIS; WEGENERS-GRANULOMATOSIS; PLASMA-MEMBRANE; MEDIATED GLOMERULONEPHRITIS;

D O I：

10.1111/j.1365-2249.2012.04615.x

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

OTHER ARTICLES PUBLISHED ON ANCA IN THIS ISSUE Animal models of anti-neutrophil cytoplasmic antibody-associated vasculitis. Clinical and Experimental Immunology 2012, 169: 22937. Summary Neutrophils are pivotal to host defence during infectious diseases. However, activated neutrophils may also cause undesired tissue damage. Ample examples include small-vessel inflammatory diseases (vasculitis) that are associated with anti-neutrophil cytoplasmic autoantibodies (ANCA) residing in the patients' plasma. In addition to being an important diagnostic tool, convincing evidence shows that ANCA are pathogenic. ANCAneutrophil interactions induce important cellular responses that result in highly inflammatory necrotizing vascular damage. The interaction begins with ANCA binding to their target antigens on primed neutrophils, proceeds by recruiting transmembrane molecules to initiate intracellular signal transduction and culminates in activation of effector functions that ultimately mediate the tissue damage.

引用

页码：220 / 228

页数：9

共 81 条

[1] Proteinase 3 and CD177 are expressed on the plasma membrane of the same subset of neutrophils [J].