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蛋白酶3同源细菌蛋白酶在小鼠中诱导蛋白酶3-抗中性粒细胞胞浆自身抗体

Induction of proteinase 3-anti-neutrophil cytoplasmic autoantibodies by proteinase 3-homologous bacterial protease in mice.

作者信息

Kim Yong Chul, Choi Yun Sik, Alam Jehan, Kim Yun-Ji, Baek Keum Jin, Koh Jaemoon, Song Yeong Wook, Chung Doo-Hyun, Choi Youngnim

机构信息

Department of Oral Microbiology and Immunology, School of Dentistry and Dental Research Institute, Seoul National University, 101 Daehak-ro, Jongno-gu, Seoul, 110-744, Republic of Korea.

KSJ Probioticslab, 4 Inchon-ro 17ga-gil, Seongbuk-gu, Seoul, Republic of Korea.

出版信息

Immunol Res. 2016 Apr;64(2):438-44. doi: 10.1007/s12026-015-8687-4.

Abstract

Proteinase 3 (PR3) is the principal target of antineutrophil cytoplasmic autoantibodies (ANCA) associated with granulomatosis with polyangiitis. The aim of this study was to investigate whether bacterial PR3-homologous protease can induce autoantibodies to PR3 and ANCA-associated pathology in mice. Among the bacterial proteases that have greater than 30 % identity with PR3, a trypsin-like serine protease of Saccharomonospora viridis, a bacterium that causes hypersensitivity pneumonitis, was chosen. When the mice were immunized with the recombinant protease of S. viridis (SvPR), 75 % of NZBWF1 and 100 % of C57BL/6 mice developed high levels of autoantibodies to mouse PR3 (mPR3). The levels of antibodies to mPR3 had a strong positive correlation with those to SvPR. In addition, more than half of the mPR3-reactive sera (63 %) reacted to purified human PR3 (hPR3), and the levels of antibodies to hPR3 had a positive correlation with those to mPR3. The sera from the immunized mice strongly stained murine neutrophils in a C-ANCA pattern. Although granulomatous inflammation and signs of vasculitis were observed in several mice, they were attributable to the use of complete Freund's adjuvant in the immunization. Collectively, exposure to PR3-homologous bacterial protease could induce ANCA in mice, and this finding may provide a new insight into the triggering mechanisms for the production of PR3-ANCA.

摘要

蛋白酶3(PR3)是与肉芽肿性多血管炎相关的抗中性粒细胞胞浆自身抗体(ANCA)的主要靶标。本研究的目的是调查细菌PR3同源蛋白酶是否能在小鼠中诱导针对PR3的自身抗体及ANCA相关病理改变。在与PR3具有超过30%同源性的细菌蛋白酶中,选择了一种来自绿糖单孢菌(一种可引起超敏性肺炎的细菌)的胰蛋白酶样丝氨酸蛋白酶。当用绿糖单孢菌的重组蛋白酶(SvPR)免疫小鼠时,75%的NZBWF1小鼠和100%的C57BL/6小鼠产生了高水平的针对小鼠PR3(mPR3)的自身抗体。针对mPR3的抗体水平与针对SvPR的抗体水平呈强正相关。此外,超过一半的mPR3反应性血清(63%)与纯化的人PR3(hPR3)发生反应,并且针对hPR3的抗体水平与针对mPR3的抗体水平呈正相关。免疫小鼠的血清以C-ANCA模式强烈染色小鼠中性粒细胞。尽管在几只小鼠中观察到肉芽肿性炎症和血管炎迹象,但它们归因于免疫过程中使用了完全弗氏佐剂。总体而言,暴露于PR3同源细菌蛋白酶可在小鼠中诱导ANCA,这一发现可能为PR3-ANCA产生的触发机制提供新的见解。

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