Yoo Seung-Min, Jeon Hyungtaek, Lee Suhyuk, Lee Myung-Shin
Department of Microbiology and Immunology, Eulji University School of Medicine, Daejeon 84824, Republic of Korea.
J Microbiol Biotechnol. 2016 Mar;26(3):618-26. doi: 10.4014/jmb.1512.12031.
Pleural effusion lymphoma (PEL) is a rare B-cell lymphoma that has a very poor prognosis with a median survival time of around 6 months. PEL is caused by Kaposi's sarcoma-associated herpesvirus, and is often co-infected with the Epstein Barr virus. The complement system is fundamental in the innate immune system against pathogen invasion and tumor development. In the present study, we investigated the activation of the complement system in PEL cells using human serum complements. Interestingly, two widely used PEL cell lines, BCP-1 and BCBL-1, showed different susceptibility to the complement system, which may be due to CD46 expression on their cell membranes. Complement activation did not induce apoptosis but supported cell survival considerably. Our results demonstrated the susceptibility of PEL to the complement system and its underlying mechanisms, which would provide insight into understanding the pathogenesis of PEL.
胸腔积液淋巴瘤(PEL)是一种罕见的B细胞淋巴瘤,预后很差,中位生存时间约为6个月。PEL由卡波西肉瘤相关疱疹病毒引起,常与爱泼斯坦-巴尔病毒共同感染。补体系统在抵抗病原体入侵和肿瘤发展的先天免疫系统中至关重要。在本研究中,我们使用人血清补体研究了PEL细胞中补体系统的激活情况。有趣的是,两种广泛使用的PEL细胞系BCP-1和BCBL-1对补体系统表现出不同的敏感性,这可能是由于它们细胞膜上的CD46表达所致。补体激活并未诱导细胞凋亡,反而显著支持细胞存活。我们的结果证明了PEL对补体系统的敏感性及其潜在机制,这将为理解PEL的发病机制提供见解。