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首页> 外文期刊>Veterinary research >The comparative profile of lymphoid cells and the T and B cell spectratype of germ-free piglets infected with viruses SIV, PRRSV or PCV2
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The comparative profile of lymphoid cells and the T and B cell spectratype of germ-free piglets infected with viruses SIV, PRRSV or PCV2

机译:感染了SIV,PRRSV或PCV2病毒的无菌小猪的淋巴样细胞的对比特征以及T和B细胞光谱类型

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Lymphocyte subsets isolated from germ-free piglets experimentally infected with swine influenza virus (SIV), porcine reproductive and respiratory syndrome virus (PRRSV) or porcine circovirus type 2 (PCV2) were studied and the profile of these subsets among these three infections was monitored. Germ-free piglets were used since their response could be directly correlated to the viral infection. Because SIV infections are resolved even by colostrum-deprived neonates whereas PRRSV and PCV2 infections are not, SIV was used as a benchmark for an effectively resolved viral infection. PRRSV caused a large increase in the proportion of lymphocytes at the site of infection and rapid differentiation of B cells leading to a high level of Ig-producing cells but a severe reduction in CD2—CD21+ primed B cells. Unlike SIV and PCV2, PRRSV also caused an increase in terminally differentiated subset of CD2+CD8α+ γδ cells and polyclonal expansion of major Vβ families suggesting that non-specific helper T cells drive swift B cell activation. Distinct from infections with SIV and PRRSV, PCV2 infection led to the: (a) prevalence of MHC-II+ T cytotoxic cells, (b) restriction of the T helper compartment in the respiratory tract, (c) generation of a high proportion of FoxP3+ T cells in the blood and (d) selective expansion of IgA and IgE suggesting this virus elicits a mucosal immune response. Our findings suggest that PRRSV and PCV2 may negatively modulate the host immune system by different mechanisms which may explain their persistence.
机译:从实验感染猪流感病毒(SIV),猪繁殖与呼吸综合症病毒(PRRSV)或2型猪圆环病毒(PCV2)的无菌仔猪中分离出淋巴细胞亚群,并研究了这三种感染中这些亚群的概况。使用无胚仔猪,因为它们的反应可能与病毒感染直接相关。由于即使初乳剥夺的新生儿也可以解决SIV感染,而PRRSV和PCV2感染则不能解决,因此SIV被用作有效解决病毒感染的基准。 PRRSV导致感染部位的淋巴细胞比例大大增加,B细胞迅速分化,导致产生高水平的Ig细胞,但CD2 - CD21 +严重减少启动的B细胞。与SIV和PCV2不同,PRRSV还引起CD2 + CD8α + γδδ细胞的终末分化亚群增加以及主要Vβ家族的多克隆扩增,提示非特异性辅助T细胞迅速激活B细胞。与SIV和PRRSV感染不同,PCV2感染导致:(a)MHC-II + T细胞毒性细胞盛行,(b)呼吸道T辅助区的限制,(c )在血液中产生高比例的FoxP3 + T细胞,以及(d)IgA和IgE的选择性扩增,表明该病毒引发了粘膜免疫反应。我们的研究结果表明PRRSV和PCV2可能通过不同的机制负面调节宿主免疫系统,这可能解释了它们的持久性。

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