Escaping the immune system by DNA repair and recombination in African trypanosomes

被引:21
作者
Sima, Nuria [1 ]
McLaughlin, Emilia Jane [1 ]
Hutchinson, Sebastian [2 ,3 ]
Glover, Lucy [1 ]
机构
[1] Inst Pasteur, Dept Parasites & Insect Vectors, Trypanosome Mol Biol, 25-28 Rue Docteur Roux, F-75015 Paris, France
[2] Inst Pasteur, Dept Parasites & Insect Vectors, Trypanosome Cell Biol, 25-28 Rue Docteur Roux, F-75015 Paris, France
[3] Inst Pasteur, Dept Parasites & Insect Vectors, INSERM U1201, 25-28 Rue Docteur Roux, F-75015 Paris, France
基金
欧盟地平线“2020”;
关键词
VSG switching; DNA damage; homologous; recombination; VARIANT SURFACE GLYCOPROTEIN; VSG EXPRESSION SITE; RNA-POLYMERASE-I; BRC REPEAT NUMBER; ANTIGENIC VARIATION; HOMOLOGOUS RECOMBINATION; GENE CONVERSION; TELOMERE LENGTH; BRUCEI; MECHANISMS;
D O I
10.1098/rsob.190182
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
African trypanosomes escape the mammalian immune response by antigenic variation-the periodic exchange of one surface coat protein, in Trypanosoma brucei the variant surface glycoprotein (VSG), for an immunologically distinct one. VSG transcription is monoallelic, with only one VSG being expressed at a time from a specialized locus, known as an expression site. VSG switching is a predominantly recombination-driven process that allows VSG sequences to be recombined into the active expression site either replacing the currently active VSG or generating a 'new' VSG by segmental gene conversion. In this review, we describe what is known about the factors that influence this process, focusing specifically on DNA repair and recombination.
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页数:9
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