Knez Špela, Narat Mojca, Ogorevc Jernej
Department of Animal Science, Biotechnical Faculty, University of Ljubljana, Ljubljana, Slovenia.
Front Immunol. 2025 Jan 20;15:1490478. doi: 10.3389/fimmu.2024.1490478. eCollection 2024.
Toll-like receptors (TLRs) play an important role in the recognition of viral particles and activation of the innate immune system, but their role in SARS-CoV-2 infection is still poorly characterized. In the present study, we investigated the role of Toll-like receptor 10 (TLR10) in modulating the immune response during SARS-CoV-2 infection. The results showed that overexpression of in A549 lung epithelial cells, immunostimulated with SARS-CoV-2 proteins S and N mainly downregulated proinflammatory cytokines and interferons and affected gene expression in the cocultured THP-1 monocytes. Our results suggest that TLR10 could mediate the extent of SARS-CoV-2 infection by downregulating the release of inflammatory cytokines and chemokines such as , , , and . Modulation of expression could have implications for the treatment of patients with severe COVID-19, in whom excessive inflammation leading to the development of acute respiratory distress syndrome (ARDS) is a key feature. However, further research is needed to fully understand the impact of modulating expression on the antiviral response and the overall balance of the immune response during SARS-CoV-2 infection.
Toll样受体（TLRs）在识别病毒颗粒和激活先天免疫系统中发挥重要作用，但其在严重急性呼吸综合征冠状病毒2（SARS-CoV-2）感染中的作用仍不清楚。在本研究中，我们调查了Toll样受体10（TLR10）在SARS-CoV-2感染期间调节免疫反应中的作用。结果表明，在经SARS-CoV-2蛋白S和N免疫刺激的A549肺上皮细胞中过表达TLR10，主要下调促炎细胞因子和干扰素，并影响共培养的THP-1单核细胞中的基因表达。我们的结果表明，TLR10可通过下调白细胞介素6（IL-6）、白细胞介素8（IL-8）、肿瘤坏死因子α（TNF-α）和干扰素γ（IFN-γ）等炎性细胞因子和趋化因子的释放来介导SARS-CoV-2感染的程度。调节TLR10的表达可能对治疗重症2019冠状病毒病（COVID-19）患者有意义，在这些患者中，导致急性呼吸窘迫综合征（ARDS）的过度炎症是一个关键特征。然而，需要进一步研究以充分了解调节TLR10表达对SARS-CoV-2感染期间抗病毒反应和免疫反应总体平衡的影响。
