炭疽芽孢杆菌的磷脂酰肌醇特异性磷脂酶C可下调免疫反应。

Phosphatidylinositol-specific phospholipase C of Bacillus anthracis down-modulates the immune response.

作者信息

Zenewicz Lauren A, Wei Zhengyu, Goldfine Howard, Shen Hao

机构信息

Department of Microbiology, University of Pennsylvania School of Medicine, Philadelphia, PA 19104.

出版信息

J Immunol. 2005 Jun 15;174(12):8011-6. doi: 10.4049/jimmunol.174.12.8011.

DOI:10.4049/jimmunol.174.12.8011

PMID:15944308

Abstract

Phosphatidylinositol-specific phospholipases (PI-PLCs) are virulence factors produced by many pathogenic bacteria, including Bacillus anthracis and Listeria monocytogenes. Bacillus PI-PLC differs from Listeria PI-PLC in that it has strong activity for cleaving GPI-anchored proteins. Treatment of murine DCs with Bacillus, but not Listeria, PI-PLC inhibited dendritic cell (DC) activation by TLR ligands. Infection of mice with Listeria expressing B. anthracis PI-PLC resulted in a reduced Ag-specific CD4 T cell response. These data indicate that B. anthracis PI-PLC down-modulates DC function and T cell responses, possibly by cleaving GPI-anchored proteins important for TLR-mediated DC activation.

摘要

磷脂酰肌醇特异性磷脂酶（PI-PLCs）是许多病原菌产生的毒力因子，包括炭疽芽孢杆菌和单核细胞增生李斯特菌。炭疽芽孢杆菌的PI-PLC与单核细胞增生李斯特菌的PI-PLC不同，在于它对切割GPI锚定蛋白具有很强的活性。用炭疽芽孢杆菌而非单核细胞增生李斯特菌的PI-PLC处理小鼠树突状细胞（DC），可抑制TLR配体介导的树突状细胞（DC）活化。用表达炭疽芽孢杆菌PI-PLC的李斯特菌感染小鼠，导致抗原特异性CD4 T细胞反应减弱。这些数据表明，炭疽芽孢杆菌PI-PLC可能通过切割对TLR介导的DC活化很重要的GPI锚定蛋白，下调DC功能和T细胞反应。