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系统性 CD4 细胞毒性 T 细胞可提高对 PRRSV-1 经胎盘感染的保护作用。

Systemic CD4 cytotoxic T cells improve protection against PRRSV-1 transplacental infection.

机构信息

Departament de Sanitat i Anatomia Animals, Facultat de Veterinària, Universitat Autònoma de Barcelona (UAB), Cerdanyola del Vallès, Spain.

Centre de Recerca en Sanitat Animal, Institut de Recerca en Tecnologies Agroalimentáries (IRTA-CReSA), Universitat Autònoma de Barcelona (UAB), Cerdanyola del Vallès, Spain.

出版信息

Front Immunol. 2023 Jan 17;13:1020227. doi: 10.3389/fimmu.2022.1020227. eCollection 2022.

DOI:10.3389/fimmu.2022.1020227
PMID:36798517
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9928156/
Abstract

BACKGROUND

(PRRSV) is one of the major swine pathogens causing reproductive failure in sows. Although modified-live virus (MLV) vaccines are available, only partial protection against heterologous strains is produced, thus vaccinated sows can be infected and cause transplacental infection. The immune effector mechanisms involved are largely unknown.

METHODS

The present study investigated the role of cytotoxic lymphocytes, including cytotoxic T cells (CTL), NKT, and NK cells, from blood in preventing PRRSV-1 transplacental infection in vaccinated primiparous sows (two doses vaccinated). Sows from a PRRSV-1 unstable farm were bled just before the last month of gestation (critical period for transplacental infection), then followed to determine whether sows delivered PRRSV-1-infected (n=8) or healthy (n=10) piglets. After that, functions of CTL, NKT, and NK cells in the two groups of sows were compared.

RESULTS

No difference was found through cell surface staining. But upon re-stimulation with the circulating field virus, sows that delivered healthy piglets displayed a higher frequency of virus-specific CD107a IFN-γ-producing T cells, which accumulated in the CD4 compartment including CD4 single-positive (CD4 SP) and CD4/CD8α double-positive (CD4/CD8α DP) subsets. The same group of sows also harbored a higher proportion of CD107a TNF-α-producing T cells that predominantly accumulated in CD4/CD8α double-negative (CD4/CD8α DN) subset. Consistently, CD4 SP and CD4/CD8α DN T cells from sows delivering healthy piglets had a higher virus-specific proliferative response. Additionally, in sows that delivered PRRSV-1-infected piglets, a positive correlation of virus-specific IFN-γ response with average Ct values of umbilical cords of newborn piglets per litter was observed.

CONCLUSION

Our data strongly suggest that CTL responses correlate with protection against PRRSV-1 transplacental infection, being executed by CD4 T cells (IFN-γ related) and/or CD4/CD8α DN T cells (TNF-α related).

摘要

背景

(PRRSV)是一种主要的猪病原体,可导致母猪繁殖失败。虽然有改良活病毒(MLV)疫苗可用,但仅对异源株产生部分保护,因此接种疫苗的母猪仍可能感染并导致胎盘感染。涉及的免疫效应机制在很大程度上尚不清楚。

方法

本研究调查了来自血液的细胞毒性淋巴细胞,包括细胞毒性 T 细胞(CTL)、NKT 和 NK 细胞,在预防接种初产母猪(接种两剂)的 PRRSV-1 胎盘感染中的作用。来自 PRRSV-1 不稳定农场的母猪在妊娠最后一个月前(胎盘感染的关键时期)采血,然后跟踪确定母猪是否产下 PRRSV-1 感染(n=8)或健康(n=10)仔猪。之后,比较了两组母猪的 CTL、NKT 和 NK 细胞的功能。

结果

通过细胞表面染色未发现差异。但是,在用循环田间病毒再刺激后,产下健康仔猪的母猪显示出更高频率的病毒特异性 CD107a IFN-γ产生 T 细胞,这些细胞在包括 CD4 单阳性(CD4 SP)和 CD4/CD8α 双阳性(CD4/CD8α DP)亚群在内的 CD4 区室中积累。同一组母猪还具有更高比例的 CD107a TNF-α产生 T 细胞,主要在 CD4/CD8α 双阴性(CD4/CD8α DN)亚群中积累。一致地,来自产下健康仔猪的母猪的 CD4 SP 和 CD4/CD8α DN T 细胞具有更高的病毒特异性增殖反应。此外,在产下 PRRSV-1 感染仔猪的母猪中,观察到病毒特异性 IFN-γ反应与每窝新生仔猪脐带的平均 Ct 值之间存在正相关。

结论

我们的数据强烈表明,CTL 反应与 PRRSV-1 胎盘感染的保护作用相关,由 CD4 T 细胞(与 IFN-γ相关)和/或 CD4/CD8α DN T 细胞(与 TNF-α相关)执行。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/bceac0114d2f/fimmu-13-1020227-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/0fb82d09c76b/fimmu-13-1020227-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/6b5d5abb60d5/fimmu-13-1020227-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/b4f7cb6c015f/fimmu-13-1020227-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/c76c9f003ae4/fimmu-13-1020227-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/a36a1c87a6c6/fimmu-13-1020227-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/92b53120f661/fimmu-13-1020227-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/bceac0114d2f/fimmu-13-1020227-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/0fb82d09c76b/fimmu-13-1020227-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/6b5d5abb60d5/fimmu-13-1020227-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/b4f7cb6c015f/fimmu-13-1020227-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/c76c9f003ae4/fimmu-13-1020227-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/a36a1c87a6c6/fimmu-13-1020227-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/92b53120f661/fimmu-13-1020227-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/829d/9928156/bceac0114d2f/fimmu-13-1020227-g007.jpg

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