Natural killer and dendritic cell contact in lesional atopic dermatitis skin -: Malassezia-influenced cell interaction

Natural killer and dendritic cell contact in lesional atopic dermatitis skin -: Malassezia-influenced cell interaction
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DOI:
10.1046/j.1523-1747.2002.00132.x
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发表时间:
2002-10-01
影响因子:
6.5
通讯作者:
Scheynius, A
Scheynius, A
中科院分区:
医学1区
文献类型:
--
作者:
Buentke, E;Heffler, LC;Scheynius, A

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树突状细胞的调控机制还远未完全明了。有趣的是,最近的几份报告表明,自然杀伤细胞在影响树突状细胞的成熟和细胞之间直接接触时的功能方面发挥了作用。目前尚不清楚这种相互作用是否也在体内发生,或者自然杀伤细胞和树突状细胞之间的潜在相互作用是否会受到树突状细胞的过敏原暴露的影响。酵母菌马拉色菌可作为特应性湿疹/皮炎综合征的过敏原,并诱导树突状细胞成熟。我们的目的是研究特应性湿疹/皮炎综合征患者皮肤中自然杀伤细胞的分布,重点是自然杀伤细胞与树突状细胞之间可能的相互作用,并评估马拉色菌与树突状细胞的相互作用是否会影响树突状细胞和自然杀伤细胞之间的后续相互作用。在正常人真皮和特应性湿疹/皮炎综合征患者的非皮损皮肤中发现少量散在的自然杀伤细胞(CD56(+)/CD3(-))。然而,在皮损皮肤和马拉色菌斑贴试验阳性皮肤活检中,自然杀伤细胞是不同分布的,我们第一次可以显示自然杀伤细胞和CD1a(+)树突状细胞之间的密切接触。与马拉色菌预先孵育的树突状细胞对自然杀伤细胞诱导的细胞死亡不那么敏感,这表明马拉色菌对树突状细胞与自然杀伤细胞的相互作用有直接影响。这些发现表明,自然杀伤细胞和树突状细胞可以在皮肤中相互作用,马拉色菌影响自然杀伤细胞和树突状细胞之间的相互作用。我们的数据表明,自然杀伤细胞可能在特应性湿疹/皮炎综合征的树突状细胞调节中发挥作用。
The regulation of dendritic cells is far from fully understood. Interestingly, several recent reports have suggested a role for natural killer cells in affecting dendritic cell maturation and function upon direct contact between the cells. It is not known if this interaction takes place also in vivo, or if a potential interaction of natural killer cells and dendritic cells would be affected by allergen exposure of the dendritic cells. The yeast Malassezia can act as an allergen in atopic eczema/dermatitis syndrome, and induce maturation of dendritic cells. Our aims were to study the distribution of natural killer cells in the skin from atopic eczema/dermatitis syndrome patients with the emphasis on possible natural killer cell-dendritic cell interaction, and to assess whether the interaction of Malassezia with dendritic cells would affect subsequent interaction between dendritic cells and natural killer cells. A few scattered natural killer (CD56(+)/CD3(-)) cells were found in the dermis of healthy individuals and in nonlesional skin from atopic eczema/dermatitis syndrome patients. In lesional skin and in biopsies from Malassezia atopy-patch-test-positive skin, however, natural killer cells were differentially distributed and for the first time we could show close contact between natural killer cells and CD1a(+) dendritic cells. Dendritic cells preincubated with Malassezia became less susceptible to natural-killer-cell-induced cell death, suggesting a direct effect imposed by Malassezia upon interaction of dendritic cells with natural killer cells. These findings indicate that natural killer cells and dendritic cells can interact in the skin and that Malassezia affects the interaction between natural killer cells and dendritic cells. Our data suggest that natural killer cells may play a role in regulating dendritic cells in atopic eczema/dermatitis syndrome.