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首页> 外文期刊>Journal of interferon and cytokine research: The official journal of the International Society for Interferon and Cytokine Research >The receptor for type I IFNs is highly expressed on peripheral blood B cells and monocytes and mediates a distinct profile of differentiation and activation of these cells.
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The receptor for type I IFNs is highly expressed on peripheral blood B cells and monocytes and mediates a distinct profile of differentiation and activation of these cells.

机译：I型IFN的受体在外周血B细胞和单核细胞上高表达，并介导这些细胞分化和激活的独特特征。

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Type I interferons (IFNs) are potent regulators of both innate and adaptive immunity. All type I IFNs bind to the same heterodimeric cell surface receptor composed of IFN-alpha receptor (IFNAR-1) and IFN-alpha/beta receptor (IFNAR-2) polypeptides. This study revealed that type I IFN receptor levels vary considerably on hematopoietic cells, with monocytes and B cells expressing the highest levels. Overnight treatment of peripheral blood mononuclear cells (PBMCs) with IFN-alpha2b or IFN-beta led to increased expression on monocytes and B cells of surface markers commonly associated with activated antigen-presenting cells (APCs), such as CD38, CD86, MHC class I, and MHC class II. Five-day exposure of adherent monocytes to granulocyte-macrophage colony-stimulating factor (GM-CSF) plus IFN-alpha or IFN-beta caused the development of potent allostimulatory cells with morphology similar to that of myeloid dendritic cells (DCs) obtained from culture with GM-CSF and interleukin-4 (IL-4) but with distinct cell surface marker profiles and activity. In contrast to IL-4-derived DCs, IFN-alpha-derived DCs were CD14+, CD1a-, CD123+, CD32+, and CD38+ and expressed high levels of CD86 and MHC class II. Development of these cells was completely blocked by an antibody to IFNAR-1. Furthermore, activity of the type I IFN-derived DC in a mixed lymphocyte reaction (MLR) was consistently more potent than that of IL-4-derived DCs, especially at high responder/stimulator ratios. This MLR activity was abrogated by the addition of anti-IFNAR-1 antibody at the start of the DC culture. In contrast, there was no effect of anti-IFNAR-1 on IL-4-derived DCs, indicating that this is a distinct pathway of DC differentiation. These results suggest a potential role for anti-IFNAR-1 immunotherapy in autoimmune diseases, such as systemic lupus erythematosus (SLE), in which the action of excessive type I IFN on B cells and myeloid DCs may play a role in disease pathology.
机译：I型干扰素（IFN）是先天免疫和适应性免疫的有效调节剂。所有I型IFN均与由IFN-α受体（IFNAR-1）和IFN-α/β受体（IFNAR-2）多肽组成的同一异二聚体细胞表面受体结合。这项研究表明，I型IFN受体水平在造血细胞上有很大差异，其中单核细胞和B细胞表达水平最高。用IFN-alpha2b或IFN-beta过夜处理外周血单核细胞（PBMC）导致单核细胞和B细胞上与活化抗原呈递细胞（APC）通常相关的表面标志物（例如CD38，CD86，MHC类）的表达增加I和MHC II级。粘附单核细胞与粒细胞-巨噬细胞集落刺激因子（GM-CSF）加上IFN-α或IFN-β接触五天会导致形成强大的同种异体刺激细胞，其形态类似于从培养物中获得的髓样树突状细胞（DC）具有GM-CSF和白介素4（IL-4），但具有明显的细胞表面标志物特征和活性。与IL-4衍生的DC相比，IFN-α衍生的DC为CD14 +，CD1a-，CD123 +，CD32 +和CD38 +，并表达高水平的CD86和II类MHC。这些细胞的发育被IFNAR-1抗体完全阻断。此外，混合淋巴细胞反应（MLR）中I型IFN衍生的DC的活性始终比IL-4衍生的DC的活性更高，尤其是在高响应者/刺激者比率下。通过在DC培养开始时添加抗IFNAR-1抗体来消除这种MLR活性。相反，抗IFNAR-1对IL-4衍生的DC没有作用，表明这是DC分化的​​独特途径。这些结果表明抗IFNAR-1免疫疗法在自身免疫疾病（例如系统性红斑狼疮（SLE））中的潜在作用，其中过量的I型干扰素对B细胞和髓样DC的作用可能在疾病病理中起作用。

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