Templeton Thomas J
Department of Microbiology and Immunology, Weill Cornell Medical College, New York, NY 10021, USA.
Mol Biochem Parasitol. 2009 Aug;166(2):109-16. doi: 10.1016/j.molbiopara.2009.04.003. Epub 2009 Apr 16.
The human malaria parasite, Plasmodium falciparum, is able to evade host cell-mediated and humoral immunity to maintain both persistent and repeated infections. Immune evasion is in part due to a robust repertoire of proteins which participate in host-parasite interactions but also exhibit profound antigenic diversity, and in some instances switches in gene expression. The antigenic diversity occurs both at the parasite level within families of amplified proteins, and within populations of parasites in which mechanisms of recombination and gene conversion conspire to create a broad plasticity in the antigenic exposure to the host. This review will introduce the spectrum of amplified protein families in P. falciparum and focus on three sub-telomeric encoded families, RIFIN, STEVOR and Pfmc-2TM which exhibit hypervariability with respect to their antigenic diversity.
人类疟原虫恶性疟原虫能够逃避宿主细胞介导的免疫和体液免疫，从而维持持续性和复发性感染。免疫逃避部分归因于一系列丰富的蛋白质，这些蛋白质参与宿主-寄生虫相互作用，但也表现出深刻的抗原多样性，并且在某些情况下会发生基因表达的转换。抗原多样性既发生在扩增蛋白家族内的寄生虫水平，也发生在寄生虫群体中，在这些群体中，重组和基因转换机制共同作用，在宿主的抗原暴露方面产生广泛的可塑性。本综述将介绍恶性疟原虫中扩增蛋白家族的范围，并重点关注三个亚端粒编码家族，即RIFIN、STEVOR和Pfmc-2TM，它们在抗原多样性方面表现出高度变异性。
