Chlamydia pneumoniae secretion of a protease-like activity factor for degrading host cell transcription factors is required for complex antigen expression
Chlamydia pneumoniae secretion of a protease-like activity factor for degrading host cell transcription factors is required for complex antigen expression
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DOI：
10.1128/iai.70.1.345-349.2002
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发表时间：
2002-01-01
影响因子：
3.1
通讯作者：
Zhong, GM
中科院分区：
文献类型：
--
作者：
Fan, PY;Dong, F;Zhong, GM
肺炎衣原体是许多呼吸道感染的病原体，并与人类心血管疾病有关。C.认为肺炎链球菌依赖于其引起持续感染和逃避宿主防御的能力。基因组序列分析表明，肺炎衣原体编码一个同源的衣原体蛋白酶样活性因子从沙眼衣原体（CPAFct）。我们指定了C。pneumoniae同源物CPAFcp。重组CPAFcp的生产和发现降解RFX 5，所需的主要组织相容性复合物（MHC）抗原表达的宿主转录因子。降解是可逆的lactacystin，一种不可逆的蛋白酶体抑制剂。此外，CPA-Fcp还可被C.肺炎菌C的耗尽。肺炎衣原体分泌的CPAFcp与特异性抗体一起完全消除了感染细胞中RFX 5的降解活性，表明CPAFcp是在C.肺炎感染。这些观察揭示了C. pneumoniae病毒逃避宿主的适应性免疫，这可能有助于其持久性。
Chlamydia pneumoniae is a causative agent for many respiratory infections and has been associated with cardiovascular diseases in humans. The pathogenicity of C. pneumoniae is thought to depend on its ability to cause persistent infection and to evade host defense. Genome sequence analysis indicates that C pneumoniae encodes a homologue of a chlamydial protease-like activity factor from C trachomatis (CPAFct). We designated the C. pneumoniae homologue as CPAFcp. Recombinant CPAFcp was produced and found to degrade RFX5, a host transcription factor required for major histo compatibility complex (MHC) antigen expression. The degradation was inhibitable by lactacystin, an irreversible proteasome inhibitor. Furthermore, CPA-Fcp was secreted into host cytosol by C. pneumoniae organisms. Depletion of the C. pneumoniae-secreted CPAFcp with specific antibodies completely ablated the RFX5 degradation activity in the infected cells, suggesting that CPAFcp is necessary for the degradation of host transcription factors required for MHC antigen expression during C. pneumoniae infection. These observations have revealed a unique molecular mechanism for C. pneumoniae to evade host adaptive immunity that may aid in its persistence.