Co-infection of porcine dendritic cells with porcine circovirus type 2a (PCV2a) and genotype II porcine reproductive and respiratory syndrome virus (PRRSV) induces CD4(+)CD25(+)FoxP3(+) T cells in vitro.

Co-infection of porcine dendritic cells with porcine circovirus type 2a (PCV2a) and genotype II porcine reproductive and respiratory syndrome virus (PRRSV) induces CD4(+)CD25(+)FoxP3(+) T cells in vitro.
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DOI:
10.1016/j.vetmic.2012.04.040
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发表时间:
2012-11-09
影响因子:
3.3
通讯作者:
Leroith T
Leroith T
中科院分区:
农林科学2区
文献类型:
--
作者:
Cecere TE;Meng XJ;Pelzer K;Todd SM;Beach NM;Ni YY;Leroith T

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猪圆环病毒相关疾病(Porcine Circovirus associated disease,PCVAD)是目前世界养猪业中最具经济意义的疾病之一。猪圆环病毒2型(PCV 2)是主要的病原体,然而,与其他猪病原体如猪繁殖与呼吸综合征病毒(PRRSV)的共感染通常需要诱导临床PCVAD的全谱。虽然导致临床疾病的病毒共感染的具体机制尚未完全了解,但共感染病毒的免疫调节可能起着关键作用。我们评估了用PRRSV、PCV 2或两者感染的树突状细胞(DC)体外诱导调节性T细胞(T细胞)的能力。用PCV 2感染的DC显著增加了CD 4 + CD 25 + FoxP 3 + T细胞(p < 0.05),并且用PRRSV和PCV 2共感染的DC比单独用PCV 2感染的DC诱导了显著更高数量的T细胞(p < 0.05)。细胞因子分析表明,共感染的DC诱导的TcB可能依赖于TGF-β而不是IL-10。我们的数据支持PCV 2/PRRSV共感染在PCVAD发病机制中的免疫调节作用,特别是通过Treg介导的免疫抑制。
Porcine circovirus associated disease (PCVAD) is currently one of the most economically important diseases in the global swine industry. Porcine circovirus type 2 (PCV2) is the primary causative agent, however co-infection with other swine pathogens such as porcine reproductive and respiratory syndrome virus (PRRSV) is often required to induce the full spectrum of clinical PCVAD. While the specific mechanisms of viral co-infection that lead to clinical disease are not fully understood, immune modulation by the co-infecting viruses likely plays a critical role. We evaluated the ability of dendritic cells (DC) infected with PRRSV, PCV2, or both to induce regulatory T cells (Tregs) in vitro. DCs infected with PCV2 significantly increased CD4+CD25+FoxP3+ Tregs (p < 0.05) and DCs co-infected with PRRSV and PCV2 induced significantly higher numbers of Tregs than with PCV2 alone (p < 0.05). Cytokine analysis indicated that the induction of Tregs by co-infected DCs may be dependent on TGF-β and not IL-10. Our data support the immunomodulatory role of PCV2/PRRSV co-infection in the pathogenesis of PCVAD, specifically via Treg-mediated immunosuppression.
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