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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Human Langerhans cells induce distinct IL-22-producing CD4~+ T cells lacking IL-17 production
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Human Langerhans cells induce distinct IL-22-producing CD4~+ T cells lacking IL-17 production

机译：人类朗格汉斯细胞诱导缺乏IL-17产生的独特的产生IL-22的CD4〜+ T细胞

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摘要

IL-22 is a cytokine that acts mainly on epithelial cells. In the skin, it mediates keratinocyte proliferation and epidermal hyperplasia and is thought to play a central role in inflammatory diseases with marked epidermal acanthosis, such as psoriasis. Although IL-22 was initially considered a Th17 cytokine, increasing evidence suggests that T helper cells can produce IL-22 even without IL-17 expression. In addition, we have shown the existence of this unique IL-22-producing T cell in normal skin and in the skin of psoriasis and atopic dermatitis patients. In the present study, we investigated the ability of cutaneous resident dendritic cells (DCs) to differentiate IL-22-producing cells. Using FACS, we isolated Langerhans cells (LCs; HLA-DR~+CD207~+ cells) and dermal DCs (HLA-DR~(hi)CD11c~+BDCA-1~+ cells) from normal human epidermis and dermis, respectively. Both LCs and dermal DCs significantly induced IL-22-producing CD4~+ and CD8~+ T cells from peripheral blood T cells and naive CD4~+ T cells in mixed leukocyte reactions. LCs were more powerful in the induction of IL-22-producing cells than dermal DCs. Moreover, in vitro-generated LC-type DCs induced IL-22-producing cells more efficiently than monocyte-derived DCs. The induced IL-22 production was more correlated with IFN-γ than IL-17. Surprisingly, the majority of IL-22-producing cells induced by LCs and dermal DCs lacked the expression of IL-17, IFN-γ, and IL-4. Thus, LCs and dermal DCs preferentially induced helper T cells to produce only IL-22, possibly "Th22" cells. Our data indicate that cutaneous DCs, especially LCs, may control the generation of distinct IL-22 producing Th22 cells infiltrating into the skin.
机译：IL-22是主要作用于上皮细胞的细胞因子。在皮肤中，它介导角质形成细胞增殖和表皮增生，被认为在具有明显表皮棘皮症的炎性疾病如牛皮癣中起重要作用。尽管最初将IL-22视为Th17细胞因子，但越来越多的证据表明，即使没有IL-17表达，T辅助细胞也可以产生IL-22。另外，我们已经证明在正常皮肤以及牛皮癣和特应性皮炎患者的皮肤中存在这种独特的产生IL-22的T细胞。在本研究中，我们调查了皮肤驻留树突状细胞（DC）区分产生IL-22的细胞的能力。使用流式细胞仪，我们分别从正常人的表皮和真皮中分离出朗格汉斯细胞（LC； HLA-DR〜+ CD207〜+细胞）和真皮DC（HLA-DR〜（hi）CD11c〜+ BDCA-1〜+细胞）。在混合白细胞反应中，LC和真皮DC均可显着诱导外周血T细胞和幼稚CD4 + T细胞中产生IL-22的CD4〜+和CD8〜+ T细胞。 LC在诱导产生IL-22的细胞方面比真皮DC更强大。此外，体外产生的LC型DC比单核细胞衍生的DC更有效地诱导产生IL-22的细胞。与IL-17相比，诱导的IL-22产生与IFN-γ的相关性更高。令人惊讶地，由LC和真皮DC诱导的大多数产生IL-22的细胞缺乏IL-17，IFN-γ和IL-4的表达。因此，LC和真皮DC优先诱导辅助T细胞仅产生IL-22，可能是“ Th22”细胞。我们的数据表明，皮肤DC，尤其是LC，可以控制渗透到皮肤的IL-22产生Th22细胞的产生。

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  • 作者

    Hideki Fujita; Kristine E. Nograles; Toyoko Kikuchi; Juana Gonzalez; John A. Carucci; James G. Krueger;

  • 作者单位

    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10065;

    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10065;

    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10065;

    Translational Immunomonitoring Resource Center, The Rockefeller University, New York, NY 10065;

    Department of Dermatology, Weill Medical College of Cornell University, New York, NY 10021;

    Laboratory for Investigative Dermatology, The Rockefeller University, New York, NY 10065;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    dermal dendritic cells; skin; Th22;

    机译：真皮树突状细胞皮肤;Th22;

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