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IRF family proteins and type Ⅰ interferon induction in dendritic cells

机译：树突状细胞中IRF家族蛋白和Ⅰ型干扰素的诱导

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Dendritic cells (DC), although a minor population in hematopoietic cells, produce type Ⅰ interferons (IFN) and other cytokines and are essential for innate immunity. They are also potent antigen presenters and regulate adaptive immunity. Among DC subtypes plasmacytoid DC (pDC) produce the highest amounts of type Ⅰ IFN. In addition, pro- and anti-inflammatory cytokines such as IL-12 and IL-10 are induced in DC in response to Toll like receptor (TLR) signaling and upon viral infection. Proteins in the IRF family control many aspects of DC activity. IRF-8 and IRF-4 are essential for DC development. They differentially control the development of four DC subsets. IRF-8~(-/-) mice are largely devoid of pDC and CD8α~+ DC, while IRF-4~(-/-) mice lack CD4~+DC. IRF-8~(-/-) IRF4~(-/-), double knock-out mice have only few CD8a ~-CD4~-DC that lack MHC II. IRF proteins also control type Ⅰ IFN induction in DC. IRF-7, activated upon TLR signaling is required for IFN induction not only in pDC, but also in conventional DC (cDC) and non-DC cell types. IRF-3, although contributes to IFN induction in fibroblasts, is dispensable in IFN induction in DC. Our recent evidence reveals that type Ⅰ IFN induction in DC is critically dependent on IRF-8, which acts in the feedback phase of IFN gene induction in DC. Type Ⅰ IFN induction in pDC is mediated by MyD88 dependent signaling pathway, and differs from pathways employed in other cells, which mostly rely on TLR3 and RIG-I family proteins. Other pro-inflammatory cytokines are produced in an IRF-5 dependent manner. However, IRF-5 is not required for IFN induction, suggesting the presence of separate mechanisms for induction of type Ⅰ IFN and other pro-inflammatory cytokines. IFN and other cytokines produced by activated DC in turn advance DC maturation and change the phenotype and function of DC. These processes are also likely to be governed by IRF family proteins.
机译：树突状细胞（DC）尽管在造血细胞中占少数，但会产生Ⅰ型干扰素（IFN）和其他细胞因子，对于先天免疫至关重要。它们还是有效的抗原呈递剂，并调节适应性免疫。在DC亚型中，浆细胞样DC（pDC）产生最高量的Ⅰ型I​​FN。另外，响应Toll样受体（TLR）信号转导和病毒感染，在DC中诱导促炎和抗炎细胞因子，例如IL-12和IL-10。 IRF家族中的蛋白质控制着DC活性的许多方面。 IRF-8和IRF-4对于DC开发至关重要。它们以差异方式控制四个DC子集的发展。 IRF-8〜（-/-）小鼠缺乏pDC和CD8α〜+ DC，而IRF-4〜（-/-）小鼠缺乏CD4〜+ DC。 IRF-8〜（-/-）IRF4〜（-/-），双敲除小鼠只有少数缺少MHC II的CD8a〜-CD4〜-DC。 IRF蛋白还控制DC中的Ⅰ型IFN诱导。不仅在pDC中，而且在常规DC（cDC）和非DC细胞类型中，IFN诱导均需要通过TLR信号激活的IRF-7。 IRF-3尽管有助于成纤维细胞中的IFN诱导，但在DC中的IFN诱导中却是不可缺少的。我们最近的证据表明，DC中的Ⅰ型IFN诱导严重依赖于IRF-8，它在DC中的IFN基因诱导的反馈阶段起作用。 pDC中的Ⅰ型IFN诱导是通过MyD88依赖性信号传导途径介导的，与其他细胞中使用的途径不同，后者主要依赖TLR3和RIG-1家族蛋白。其他促炎细胞因子以IRF-5依赖性方式产生。但是，IRF-5并不是诱导IFN所必需的，提示存在单独的机制来诱导Ⅰ型IFN和其他促炎性细胞因子。激活的DC产生的IFN和其他细胞因子会进一步促进DC成熟，并改变DC的表型和功能。这些过程也可能由IRF家族蛋白控制。

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