Human epidermal Langerhans cells differ from monocyte-derived Langerhans cells in CD80 expression and in secretion of IL-12 after CD40 cross-linking
Human epidermal Langerhans cells differ from monocyte-derived Langerhans cells in CD80 expression and in secretion of IL-12 after CD40 cross-linking
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DOI：
10.1189/jlb.0703327
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发表时间：
2004-09-01
影响因子：
5.5
通讯作者：
Kolde, G
中科院分区：
文献类型：
--
作者：
Peiser, M;Wanner, R;Kolde, G
朗格汉斯细胞（LC）代表骨髓树突状细胞（DC）的未成熟群体。由于其独特的Birbeck颗粒（BG），langerin表达和异质性成熟过程，它们不同于其他未成熟DC。单核细胞衍生的LC（MoLC）模拟表皮LC。通过用粒细胞巨噬细胞集落刺激因子、白细胞介素（IL）-4和转化生长因子-β 1培养血液来源的单核细胞来产生具有特征性BG的MoLC。在这里，我们比较成熟诱导的抗原表达和细胞因子释放的LC与MoLC。为了获得可比较的细胞群体，通过CD 1c细胞分选分离LC和MoLC，得到高纯度。在未刺激的细胞中，CD 40以相等水平表达。在用CD 40配体（CD 40 L）刺激后，LC和MoLC获得CD 83并增加CD 86。高CD 80表达仅在CD 1c分选的MoLC中检测到。人类白细胞抗原-DR和CD 54的表达被发现在所有的细胞群体，但是，在不同的强度。CD 40触发增加LC和MoLC刺激CD 4（+）T细胞增殖的效力。活化的MoLC释放IL-12 p70，同时释放抗炎性IL-10。Toll样受体配体肽聚糖，鞭毛蛋白，特别是脂多糖（LPS）的应用增加了这些细胞因子的共同释放。LC以与MoLC相当的水平分泌IL-10，但在施加危险信号后未能产生大量的IL-12 p70。这些数据表明，MoLC以及LC显示没有关于CD 83和CD 86表达的成熟停滞。与MoLCs不同，LCs在IL-12产生方面抵抗CD 40 L和LPS的活化。这表明自然和生成的LC具有相似的特征，但相关功能不同。
Langerhans cells (LCs) represent an immature population of myeloid dendritic cells (DCs). As a result of their unique Birbeck granules (BGs), langerin expression, and heterogeneous maturation process, they differ from other immature DCs. Monocyte-derived LCs (MoLCs) mimic epidermal LCs. MoLCs with characteristic BGs are generated by culturing blood-derived monocytes with granulocyte macrophage-colony stimulating factor, interleukin (IL)-4, and transforming growth factor-beta1. Here, we compare maturation-induced antigen expression and cytokine release of LCs with MoLCs. To achieve comparable cell populations, LCs and MoLCs were isolated by CD I c cell sorting, resulting in high purity. In unstimulated cells, CD40 was expressed at equal levels. After stimulation with CD40 ligand (CD40L), LCs and MoLCs acquired CD83 and increased CD86. High CD80 expression was exclusively detected in CD1c-sorted MoLCs. Human leukocyte antigen-DR and CD54 expression was found in all cell populations, however, at different intensities. CD40 triggering increased the potency of LCs and MoLCs to stimulate CD4(+) T cell proliferation. Activated MoLCs released IL-12p70 and simultaneously, anti-inflammatory IL-10. The application of the Toll-like receptor ligands peptidoglycan, flagellin, and in particular, lipoplysaccharide (LPS) increased the corelease of these cytokines. LCs secreted IL-10 at a comparable level with MoLCs but failed to produce high amounts of IL-12p70 after application of danger signals. These data indicate that MoLCs as well as LCs display no maturation arrest concerning CD83 and CD86 expression. In difference to MoLCs, LCs resisted activation by CD40L and LPS in terms of IL-12 production. This shows that natural and generated LCs share similar features but differ in relevant functions.