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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >IFNalpha treatment generates antigen-presenting cells insensitive to atorvastatin inhibition of MHC-II expression.
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IFNalpha treatment generates antigen-presenting cells insensitive to atorvastatin inhibition of MHC-II expression.

机译：IFNalpha处理产生对阿托伐他汀抑制MHC-II表达不敏感的抗原呈递细胞。

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摘要

IFNalpha is an immunostimulatory cytokine involved in the development of autoimmunity. Atorvastatin, a cholesterol-lowering drug, also possess immunomodulatory effects, being able to downregulate IFNgamma-induced MHC-II expression. In this study we evaluated the role of IFNalpha in monocyte differentiation to antigen-presenting cells (APCs) and the effect of atorvastatin during this process. Results showed that IFNalpha-treated monocytes differentiated into dendritic-like cells (IFNalpha-DLCs) characterized by a CD86(high), CD1a(low), MHC-II(high) and CD14(low) expression, consistent with the phenotype of mature DCs and with similar ability to uptake antigens and induce T cell responses to mature IL-4/GM-CSF-DCs. Interestingly enough, the presence of atorvastatin did not inhibit IFNalpha-induced HLA-DR expression, although this drug markedly reduced the ability of IFNalpha-DLCs to induce T cell responses. These results confirm the immunostimulatory role of IFNalpha by promoting the generation of APCs and provide new clinical applications of statins as modulators of autoimmune responses in patients with high pathological or pharmacological IFNalpha levels.
机译：IFNalpha是一种参与自身免疫发展的免疫刺激性细胞因子。阿托伐他汀是一种降低胆固醇的药物，也具有免疫调节作用，能够下调IFNγ诱导的MHC-II表达。在这项研究中，我们评估了IFNalpha在单核细胞向抗原呈递细胞（APC）分化中的作用以及阿托伐他汀在此过程中的作用。结果显示，用IFNalpha处理的单核细胞分化为树突状细胞（IFNalpha-DLCs），其特征是CD86（高），CD1a（低），MHC-II（高）和CD14（低）表达，与成熟的表型一致DC具有类似的摄取抗原并诱导对成熟IL-4 / GM-CSF-DC的T细胞应答的能力。有趣的是，阿托伐他汀的存在并未抑制IFNalpha诱导的HLA-DR表达，尽管该药物显着降低了IFNalpha-DLC诱导T细胞反应的能力。这些结果通过促进APC的产生证实了IFNα的免疫刺激作用，并为高病理或药理IFNα水平的患者提供了他汀类作为自身免疫应答调节剂的新临床应用。

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