LeRoith T, Hammond S, Todd S M, Ni Y, Cecere T, Pelzer K D
Department of Biomedical Sciences and Pathobiology, Center for Molecular Medicine and Infectious Diseases, Virginia-Maryland Regional College of Veterinary Medicine, Blacksburg, VA 24060, USA.
Vet Immunol Immunopathol. 2011 Apr 15;140(3-4):312-6. doi: 10.1016/j.vetimm.2010.12.011. Epub 2011 Jan 8.
The lack of heterologous protection by porcine reproductive and respiratory syndrome virus (PRRSV) vaccines is currently a major problem in the field. Heterologous protection by PRRS vaccines depends on the ability of the vaccine to induce an interferon gamma (IFN-γ) response. One mechanism by which the virus evades the immune system is by activating regulatory T cells (T(regs)), resulting in induction of interleukin 10 rather than IFN-γ. Our hypothesis that current PRRS vaccines do not differ from pathogenic strains in the ability to induce T(regs) was tested by inoculating three groups of pigs with two pathogenic viruses and an attenuated vaccine strain and evaluating the number of T(regs) in peripheral blood mononuclear cells. Before inoculation, the pigs, although vaccinated became infected naturally with Mycoplasma hyopneumoniae before shipment to our research facility. Our results show that the PRRSV vaccine strain and parent strain are equally able to induce T(regs) in pigs naturally infected with M. hyopneumoniae. Pigs in the vaccine and PRRSV groups had higher lung lesion scores than pigs in the control groups. The results suggest that the exacerbation M. hyopneumoniae respiratory disease may be due to the ability of PRRSV vaccination and viral infection to induce regulatory T cells.
猪繁殖与呼吸综合征病毒(PRRSV)疫苗缺乏异源保护作用,这是目前该领域的一个主要问题。PRRS疫苗的异源保护作用取决于疫苗诱导γ干扰素(IFN-γ)应答的能力。病毒逃避免疫系统的一种机制是激活调节性T细胞(Tregs),从而诱导白细胞介素10而非IFN-γ。我们的假设是,当前的PRRS疫苗在诱导Tregs的能力上与致病毒株没有差异。我们通过给三组猪接种两种致病病毒和一种减毒疫苗毒株,并评估外周血单个核细胞中Tregs的数量,来验证这一假设。在接种前,这些猪虽然已接种疫苗,但在运往我们的研究机构之前自然感染了猪肺炎支原体。我们的结果表明,PRRSV疫苗毒株和亲本毒株在诱导自然感染猪肺炎支原体的猪产生Tregs方面能力相当。疫苗组和PRRSV组的猪的肺部病变评分高于对照组的猪。结果表明,猪肺炎支原体呼吸道疾病的加重可能是由于PRRSV疫苗接种和病毒感染诱导调节性T细胞的能力所致。