Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161, Rome, Italy.
Autoimmunity. 2010 Apr;43(3):204-9. doi: 10.3109/08916930903510880.
Interferons alpha (IFNs-alpha) are pleiotropic cytokines belonging to the type I IFN family, originally described for their antiviral activity. These cytokines exhibit a long record of clinical use in patients with some types of cancer and viral diseases. Notably, certain autoimmune disorders have been postulated to be mediated by endogenous IFN-alpha and are often observed in some IFN-treated patients. IFN-alpha can induce multiple biological effects, including induction/promotion of apoptosis and inhibition of cell growth. In addition, these cytokines promote the differentiation and activity of host immune cells. Early studies in mouse tumor models showed the importance of host immune mechanisms in the generation of a long-lasting antitumor response after injection of the animals with either IFN or tumor cells genetically modified for IFN-alpha production. Several studies have shown that IFN-alpha can induce the rapid differentiation of monocytes into highly activated dendritic cells (DCs). Of note, these DCs (IFN-DCs) are particularly effective in taking up complex antigens and inducing T- and B-cell immunity. The ensemble of these results suggests that IFN-DCs can play a role in the generation of antitumor T-cell immunity, pointing out that these cells could be successfully used in strategies of cancer immunotherapy. Likewise, IFN-alpha-DC interactions could also play a role in the pathogenesis of some autoimmune disorders, often associated with IFN-alpha treatment. All this reveals the complexity of the IFN-alpha-DC interactions under normal and pathological conditions and stimulates further studies for identifying optimal modalities in either using these cytokines or controlling their production/action in patients.
干扰素 α（IFN-α）是一类具有多种生物学活性的细胞因子，属于 I 型干扰素家族，最初因其抗病毒活性而被描述。这些细胞因子在某些类型的癌症和病毒疾病患者的临床应用中有着悠久的历史。值得注意的是，某些自身免疫性疾病被认为是由内源性 IFN-α介导的，并且经常在一些接受 IFN 治疗的患者中观察到。IFN-α 可诱导多种生物学效应，包括诱导/促进细胞凋亡和抑制细胞生长。此外，这些细胞因子促进宿主免疫细胞的分化和活性。早期在小鼠肿瘤模型中的研究表明，在给动物注射 IFN 或经基因修饰可产生 IFN-α的肿瘤细胞后，宿主免疫机制在产生持久的抗肿瘤反应中具有重要作用。多项研究表明，IFN-α可诱导单核细胞迅速分化为高度活化的树突状细胞（DC）。值得注意的是，这些 DC（IFN-DC）在摄取复杂抗原和诱导 T 细胞和 B 细胞免疫方面特别有效。这些结果表明 IFN-DC 可在抗肿瘤 T 细胞免疫的产生中发挥作用，指出这些细胞可成功地用于癌症免疫治疗策略。同样，IFN-α-DC 相互作用也可能在某些自身免疫性疾病的发病机制中发挥作用，这些疾病通常与 IFN-α 治疗有关。所有这些都揭示了正常和病理条件下 IFN-α-DC 相互作用的复杂性，并促使进一步研究以确定在使用这些细胞因子或控制其在患者中的产生/作用方面的最佳方式。
