ArticleVeterinary research2015
PRRSV-infected monocyte-derived dendritic cells express high levels of SLA-DR and CD80/86 but do not stimulate PRRSV-naïve regulatory T cells to proliferate.
Article in Veterinary research, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed.
- Protein M of NADC30-like PRRSV induces MARCH6-mediated K33-linked polyubiquitination of SLA-DRA.The Journal of biological chemistry · 2026Article
- Testable Candidate Immune Correlates of Protection for Porcine Reproductive and Respiratory Syndrome Virus Vaccination.Vaccines · 2023Review
- Time Series Transcriptomic Analysis of Bronchoalveolar Lavage Cells from Piglets Infected with Virulent or Low-Virulent Porcine Reproductive and Respiratory Syndrome Virus 1.Journal of virology · 2022Article
- Swine Dendritic Cell Response to Porcine Reproductive and Respiratory Syndrome Virus: An Update.Frontiers in immunology · 2021Review
- Interaction of Type 1 Porcine Reproductive and Respiratory Syndrome Virus WithFrontiers in immunology · 2021Article
- Optimal vaccination strategy against Mycoplasma hyopneumoniae, porcine reproductive and respiratory syndrome virus, and porcine circovirus type 2 in case of early M. hyopneumoniae infection.Veterinary medicine and science · 2020Article
- Porcine Reproductive and Respiratory Syndrome Virus Promotes SLA-DR-Mediated Antigen Presentation of Nonstructural Proteins To Evoke a Nonneutralizing Antibody ResponseJournal of virology · 2020Article
- Article
- The Probiotic BB12 Induces MicroRNAs Involved in Antigen Processing and Presentation in Porcine Monocyte-Derived Dendritic Cells.International journal of molecular sciences · 2020Article
- The T-Cell Response to Type 2 Porcine Reproductive and Respiratory Syndrome Virus (PRRSV).Viruses · 2019Article
- Cellular Innate Immunity against PRRSV and Swine Influenza Viruses.Veterinary sciences · 2019Review
- In vitro immune responses of porcine alveolar macrophages reflect host immune responses against porcine reproductive and respiratory syndrome viruses.BMC veterinary research · 2018Article
- The Nucleocapsid Protein and Nonstructural Protein 10 of Highly Pathogenic Porcine Reproductive and Respiratory Syndrome Virus Enhance CD83 Production via NF-κB and Sp1 Signaling Pathways.Journal of virology · 2017Article
- Mechanisms of Adaptive Immunity to Porcine Reproductive and Respiratory Syndrome Virus.Viruses · 2017Review
- Innate and adaptive immunity against Porcine Reproductive and Respiratory Syndrome Virus.Veterinary immunology and immunopathology · 2015Review
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Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In vitro generated monocyte-derived dendritic cells (moDCs) have frequently been used to study the influence of porcine reproductive and respiratory syndrome virus (PRRSV) infection on antigen presenting cells. However, obtained results have often been conflicting in regard to expression of co-stimulatory molecules and interaction with T cells. In this study we performed a detailed phenotypic characterisation of PRRSV-infected moDCs and non-infected moDCs. For CD163 and CD169, which are involved in PRRSV-entry into host cells, our results show that prior to infection porcine moDCs express high levels of CD163 but only very low levels for CD169. Following infection with either PRRSV-1 or PRRSV-2 strains after 24 h, PRRSV-nucleoprotein (N-protein)(+) and N-protein(-) moDCs derived from the same microculture were analyzed for expression of swine leukocyte antigen-DR (SLA-DR) and CD80/86. N-protein(+) moDCs consistently expressed higher levels of SLA-DR and CD80/86 compared to N-protein(-) moDCs. We also investigated the influence of PRRSV-infected moDCs on proliferation and frequency of Foxp3(+) regulatory T cells present within CD4(+) T cells in in vitro co-cultures. Neither CD3-stimulated nor unstimulated CD4(+) T cells showed differences in regard to proliferation and frequency of Foxp3(+) T cells following co-cultivation with either PRRSV-1 or PRRSV-2 infected moDCs. Our results suggest that a more detailed characterisation of PRRSV-infected moDCs will lead to more consistent results across different laboratories and PRRSV strains as indicated by the major differences in SLA-DR and CD80/86 expression between PRRSV-infected and non-infected moDCs present in the same microculture.
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