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首页> 外文期刊>Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society >IFN-alpha2a induces IP-10/CXCL10 and MIG/CXCL9 production in monocyte-derived dendritic cells and enhances their capacity to attract and stimulate CD8+ effector T cells.
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IFN-alpha2a induces IP-10/CXCL10 and MIG/CXCL9 production in monocyte-derived dendritic cells and enhances their capacity to attract and stimulate CD8+ effector T cells.

机译:IFN-alpha2a诱导单核细胞衍生的树突状细胞产生IP-10 / CXCL10和MIG / CXCL9,并增强其吸引和刺激CD8 +效应T细胞的能力。

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摘要

Type I IFNs are immunomodulatory factors that possibly influence the properties of tissue-resident dendritic cells. Here, we have investigated the capacity of IFN-alpha2a to enhance DC chemoattractive and stimulatory capacity toward CD8+ T lymphocytes. Phenotypically, IFN-alpha2a-treated DC (IFN-DC) showed an increased expression of costimulatory and antigen-presenting molecules, maintained even after withdrawal of the cytokine. IFN-alpha2a enhanced DC stimulatory capacity toward CD8+ T cells, as assessed by increased MLR responses and induction of MART-1(26-35)-specific CTLs in vitro. No functional CCR7 chemokine receptor could be induced. Instead, high amounts of IP-10/CXCL10 and MIG/CXCL9 chemokines were produced. Freshly isolated CD8+RO+ cells and PHA-activated CD8+ T cells migrated efficiently in response to IFN-DC-conditioned medium, and the migration could be inhibited by neutralizing the CXCR3 receptor on responder cells. These results suggest that type I IFNs could enhance the elicitation of class I-restricted effector functions in vivo in the periphery by modulating DC chemoattractive properties.
机译:I型干扰素是免疫调节因子,可能会影响组织驻留树突状细胞的特性。在这里,我们研究了IFN-α2a增强DC对CD8 + T淋巴细胞的化学吸引和刺激能力的能力。从表型上看,经IFN-α2a处理的DC(IFN-DC)显示出协同刺激分子和抗原呈递分子的表达增加,甚至在撤消细胞因子后也保持了这种表达。 IFN-alpha2a增强了对CD8 + T细胞的DC刺激能力,这通过增加的MLR反应和体外对MART-1(26-35)特异性CTL的诱导来评估。无法诱导功能性CCR7趋化因子受体。相反,产生了大量的IP-10 / CXCL10和MIG / CXCL9趋化因子。新鲜分离的CD8 + RO +细胞和PHA激活的CD8 + T细胞在IFN-DC条件培养基的反应下有效迁移,并且可以通过中和反应细胞上的CXCR3受体抑制迁移。这些结果表明,I型干扰素可通过调节DC的化学吸引特性,增强体内对I类限制性效应子功能的诱导。

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