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Updated: Jun 23, 2026

An In vitro Model to Study Immune Responses of Human Peripheral Blood Mononuclear Cells to Human Respiratory Syncytial Virus Infection
Published on: December 10, 2013
IL-4-mediated monocyte differentiation modulates CD163 expression and PRRSV infection
Narae Kim1, Young-Jun Ju1, Yoon-Chul Kye1
1Department of Agricultural Biotechnology, Research Institute of Agriculture and Life Sciences, Seoul National University, Seoul, Republic of Korea.
Abstract:
Host immune status critically influences susceptibility to viral infections; however, the impact of cytokine-driven innate immune differentiation on viral permissiveness remains poorly understood. Here, we investigated whether IL-4-mediated monocyte differentiation modulates porcine reproductive and respiratory syndrome virus (PRRSV) infection. Porcine monocytes were differentiated in the presence of GM-CSF with or without IL-4 to generate monocyte-derived cells (MDCs). Notably, PRRSV replication was significantly higher in MDCs generated without IL-4 compared to those differentiated in the presence of IL-4, which was strongly associated with increased CD163 expression. Consistently, CD163 expression was downregulated in an IL-4-dependent manner. Following PRRSV infection, MDCs differentiated without IL-4 exhibited reduced TNF-α production but elevated IL-6 and IL-10 levels. In addition, MDCs generated without IL-4 showed increased expression of CD80 and SLA-1 and significantly impaired the proliferation of autologous CD8+ T cells compared to MDCs differentiated with IL-4. In vivo analysis further revealed a negative correlation between plasma IL-4 levels and CD163 expression in alveolar MDCs of PRRSV-infected pigs, which was associated with increased proportions of CD8+ T cells. Collectively, these findings suggest that IL-4-mediated innate immune programming regulates cellular permissiveness to PRRSV infection and may contribute to protective host immune responses.
Insights
Interleukin-4 (IL-4) influences how monocytes develop, impacting their susceptibility to porcine reproductive and respiratory syndrome virus (PRRSV). IL-4 helps control PRRSV infection by regulating immune cell responses.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Host immune status significantly impacts viral infection susceptibility.
- The role of cytokine-driven innate immune cell differentiation in viral permissiveness is not well understood.
Purpose of the Study:
- To investigate the effect of IL-4-mediated monocyte differentiation on porcine reproductive and respiratory syndrome virus (PRRSV) infection.
- To understand how IL-4 influences innate immune cell programming and viral permissiveness.
Main Methods:
- Porcine monocytes were differentiated into monocyte-derived cells (MDCs) with or without IL-4, using GM-CSF.
- PRRSV replication, CD163 expression, cytokine production (TNF-α, IL-6, IL-10), and T cell proliferation were analyzed.
- In vivo studies correlated plasma IL-4 levels with alveolar MDC CD163 expression and CD8+ T cell proportions in PRRSV-infected pigs.
Main Results:
- PRRSV replication was significantly higher in MDCs differentiated without IL-4, associated with increased CD163 expression.
- IL-4 downregulated CD163 expression in an IL-4-dependent manner.
- MDCs without IL-4 showed reduced TNF-α but elevated IL-6/IL-10, increased CD80/SLA-1, and impaired CD8+ T cell proliferation.
- In vivo, lower IL-4 correlated with higher CD163 and fewer CD8+ T cells in PRRSV-infected pigs.
Conclusions:
- IL-4-mediated innate immune programming regulates cellular permissiveness to PRRSV.
- IL-4 may contribute to protective host immune responses against PRRSV infection by modulating monocyte differentiation and function.
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