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Platelet concentrates modulate myeloid dendritic cell immune responses

机译：血小板浓缩物调节骨髓树突细胞免疫应答

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Platelet transfusion has been reported to modulate the recipients' immune system. To date, the precise mechanism(s) driving poor patient outcomes (e.g., increased rate of mortality, morbidity, infectious complications and prolonged hospital stays) following platelet transfusion are largely undefined. To determine the potential for platelet concentrates (PC) to modulate responses of crucial immune regulatory cells, a human in vitro whole blood model of transfusion was established. Maturation and activation of human myeloid dendritic cells (mDC) and the specialized subset blood DC antigen (BDCA)3(+) DC were assessed following exposure to buffy-coat derived PC at day (D)2 (fresh) and D5 (date-of-expiry). In parallel, to model recipients with underlying viral or bacterial infection, polyinosinic: polycytidylic acid or lipopolysaccharide was added. Exposure to PC had less of an impact on mDC responses than BDCA3(+) DC responses. PC alone downregulated BDCA3(+) DC expression of co-stimulatory molecules CD40 and CD80. In the model of viral infection, PC downregulated expression of CD83, and in the bacterial model of infection, PC downregulated CD80, CD83, and CD86. PC alone suppressed mDC production of interleukin (IL)-8, IL-12 and tumor necrosis factor (TNF)-alpha and BDCA3(+) DC production of IL-8, IL-12, and IL-6. In the model of viral infection, production of IL-12 and interferon-gamma inducible protein (IP)-10 was reduced in both DC subsets, and IL-8 was reduced in BDCA3(+) DC following PC exposure. When modeling bacterial infection, PC suppressed mDC and BDCA3(+) DC production of IL-6 and IL-10 with a reduction in TNF-alpha evident in mDC. This study assessed the impact of PC "transfusion" on DC surface antigen expression and inflammatory mediator production and provided the first evidence that PC transfusion modulates blood mDC and BDCA3(+) DC maturation and activation, particularly in the models of infection. Results of this study suggest that patients who receive PC, particularly those with underlying infectious complications, may fail to establish an appropriate immune response precipitating poor patient outcomes.
机译：据报道，血小板输注可以调节受者的免疫系统。迄今为止，血小板输注后导致患者预后不良（例如死亡率、发病率、感染性并发症和住院时间延长）的确切机制在很大程度上尚不明确。为了确定血小板浓缩物（PC）调节关键免疫调节细胞反应的潜力，建立了人体外全血输血模型。在第（D）2天（新鲜）和第5天（有效期）暴露于棕黄色外套来源的PC后，评估人类髓样树突状细胞（mDC）和血液DC抗原（BDCA）3（+）特异亚群DC的成熟和激活。同时，对于潜在病毒或细菌感染的模型受体，添加聚肌苷酸：聚胞苷酸或脂多糖。与BDCA3（+）DC反应相比，PC暴露对mDC反应的影响较小。PC单独下调共刺激分子CD40和CD80的BDCA3（+）DC表达。在病毒感染模型中，PC下调CD83的表达，在细菌感染模型中，PC下调CD80、CD83和CD86的表达。PC单独抑制mDC产生白细胞介素（IL）-8、白细胞介素-12和肿瘤坏死因子（TNF）-α，以及BDCA3（+）DC产生白细胞介素-8、白细胞介素-12和白细胞介素-6。在病毒感染模型中，PC暴露后，两个DC亚群中IL-12和干扰素γ诱导蛋白（IP）-10的产生均减少，BDCA3（+）DC中IL-8的产生减少。在模拟细菌感染时，PC抑制mDC和BDCA3（+）DC产生IL-6和IL-10，mDC中TNF-α明显减少。本研究评估了PC“输血”对DC表面抗原表达和炎症介质产生的影响，并首次证明PC输血调节血液mDC和BDCA3（+）DC的成熟和激活，尤其是在感染模型中。这项研究的结果表明，接受PC治疗的患者，尤其是那些有潜在感染并发症的患者，可能无法建立适当的免疫反应，导致患者预后不佳。

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