非甾体抗炎药影响树突状细胞细胞因子的产生。
NSAIDs affect dendritic cell cytokine production.
机构信息
Department of Radiation Oncology, Radiotherapy & OncoImmunology Laboratory, Radboud Institute for Molecular Life Sciences, Radboud UMC, Nijmegen, The Netherlands.
Department of Anesthesiology, Pain and Palliative Medicine, Radboud UMC, Nijmegen, The Netherlands.
出版信息
PLoS One. 2022 Oct 13;17(10):e0275906. doi: 10.1371/journal.pone.0275906. eCollection 2022.
BACKGROUND
Immunotherapy is now considered as the new pillar in treatment of cancer patients. Dendritic cells (DCs) play an essential role in stimulating anti-tumor immune responses, as they are capable of cross-presenting exogenous tumor antigens in MHCI complexes to activate naïve CD8+ T cells. Analgesics, like non-steroid anti-inflammatory drugs (NSAIDs), are frequently given to cancer patients to help relieve pain, however little is known about their impact on DC function.
METHODS
Here, we investigated the effect of the NSAIDs diclofenac, ibuprofen and celecoxib on the three key processes of DCs required for proper CD8+ cytotoxic T cell induction: antigen cross-presentation, co-stimulatory marker expression, and cytokine production.
RESULTS
Our results show that TLR-induced pro- and anti-inflammatory cytokine excretion by human monocyte derived and murine bone-marrow derived DCs is diminished after NSAID exposure.
CONCLUSIONS
These results indicate that various NSAIDs can affect DC function and warrant further investigation into the impact of NSAIDs on DC priming of T cells and cancer immunotherapy efficacy.
背景
免疫疗法现已被视为癌症患者治疗的新支柱。树突状细胞 (DCs) 在刺激抗肿瘤免疫反应方面发挥着重要作用，因为它们能够在外源肿瘤抗原与 MHC I 复合物中交叉呈递，从而激活初始 CD8+T 细胞。止痛药，如非甾体类抗炎药 (NSAIDs)，常被给予癌症患者以帮助缓解疼痛，但人们对其对 DC 功能的影响知之甚少。
方法
在这里，我们研究了 NSAIDs 双氯芬酸、布洛芬和塞来昔布对 DC 诱导适当的 CD8+细胞毒性 T 细胞所需的三个关键过程的影响：抗原交叉呈递、共刺激标志物表达和细胞因子产生。
结果
我们的结果表明，TLR 诱导的人单核细胞衍生和鼠骨髓衍生 DC 中的促炎和抗炎细胞因子的排泄在 NSAID 暴露后减少。
结论
这些结果表明，各种 NSAIDs 可以影响 DC 功能，并需要进一步研究 NSAIDs 对 T 细胞和癌症免疫治疗功效的 DC 启动的影响。
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