ArticleBMC veterinary research2026
Ligation of the CD163 molecule inhibits the synthesis of type I and type III interferons in porcine alveolar macrophages.
Article in BMC veterinary research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundPorcine reproductive and respiratory syndrome virus (PRRSV) is a pathogen that poses a serious threat to the health of pigs worldwide. Porcine alveolar macrophages (PAMs) are the primary target cells for the replication of PRRSV. The CD163 molecule expressed on the surface of PAMs plays a crucial role in PRRSV infection by mediating viral particle uncoating and the release of genomic RNA. However, the role of CD163 in influencing the interferon (IFN) responses remains unidentified.
resultsHere, we found that in PAMs, the expression of IFN-α, IFN-β, and IFN-λ1 was downregulated by PRRSV infection, whereas the expression of interleukin-10 (IL-10) and CD163 was upregulated, suggesting that PRRSV inhibited type I and type III IFN responses. Ligation of CD163 in PAMs was found to downregulate the expression of IFN-α, IFN-β, and IFN-λ1 and upregulate the expression of IL-10, suggesting that CD163 inhibited the type I and type III IFN responses. Knockdown of CD163 in PAMs reversed the downregulation of IFN-α, IFN-β, and IFN-λ1 expression, as well as the upregulation of IL-10 expression caused by PRRSV infection.
conclusionsIn summary, our study showed that the CD163 molecule negatively regulated the IFN responses by downregulating the production levels of type I (IFN-α/β) and type III (IFN-λ1) IFNs in PAMs. It is speculated that the interaction between PRRSV and CD163 may contribute to the virus-triggered suppression of the IFN responses.
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