In vivo levels of IL-4, IL-10, TGF-β1 and IFN-γ mRNA of the peripheral blood mononuclear cells in patients with alopecia areata in comparison to those in patients with atopic dermatitis
In vivo levels of IL-4, IL-10, TGF-β1 and IFN-γ mRNA of the peripheral blood mononuclear cells in patients with alopecia areata in comparison to those in patients with atopic dermatitis
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DOI：
10.1007/s00403-006-0700-2
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发表时间：
2007-01-01
影响因子：
3
通讯作者：
Hatano, Yutaka
中科院分区：
文献类型：
--
作者：
Katagiri, Kazumoto;Arakawa, Shoko;Hatano, Yutaka
斑秃（AA）被认为是由抗原依赖性免疫应答导致的IFN-γ的异常表达支持的。另一方面，AA有时与特应性疾病并发，尽管并发的机制尚不清楚。本研究通过检测AA患者外周血单个核细胞（PBMC）Th 1、Th 2及抑制性细胞因子的mRNA水平，探讨AA的免疫状态及其与特应性皮炎（AD）的相似性。采用半定量RT-PCR方法检测47例AA患者、15例AD患者和12例健康对照者外周血单个核细胞（PBMC）中细胞因子mRNA水平。AA患者IL-4、IFN-γ和TGF-β 1 mRNA水平低于HC患者。AA组IL-10 mRNA水平与HC组相当。AD患者的IFN-γ和TGF-β 1水平也降低。这些结果表明，基于细胞因子谱，AD和AA之间具有相似性（IFN-γ和TGF-β 1水平降低）。此外，AA中IL-4 mRNA水平的降低也可能解释了在大多数情况下与AA同时发生的特应性疾病的严重程度是轻微的。接下来，我们比较了这些细胞因子mRNA在AA的三个亚组中的水平，这些亚组根据症状的严重程度进行分类：轻度，重度和完全。虽然在任何亚组组合之间没有显著差异，但根据脱发的严重程度，有增加IFN-γ mRNA水平和降低IL-4 mRNA水平的趋势。然而，IFN-γ mRNA的水平在任何亚组低于HC。这些结果表明，IFN-γ因此参与AA的发病机制，虽然从PBMC的信息是有限的。总之，AA可能是由IFN-γ在PBMC产生低量IFN-γ和TGF-β 1的个体中的异常表达诱导的。因此，需要进一步的分析，以研究在PBMC中的群体的表型与或不与调节性T细胞的参考。
Alopecia areata (AA) has been considered to be supported by an aberrant expression of IFN-gamma as a result of antigen dependent immune response. On the other hand, AA sometimes concurs with atopic diseases, although the mechanism of the concurrence is not clear. This study was designed to elucidate the immune status of AA and the similarity between AA and atopic dermatitis (AD) by analysis of in vivo levels of mRNA of Th1, Th2, and suppressive cytokines of peripheral blood mononuclear cells (PBMC). Using semiquantitative RT-PCR, the levels of cytokine mRNA were measured in freshly isolated PBMC of 47 patients with AA, 15 patients with AD, and 12 healthy controls (HC). The levels of IL-4, IFN-gamma, and TGF-beta 1 mRNA were lower in patients with AA than those in HC. The levels of IL-10 mRNA in AA were comparable with those in HC. Decreased levels of IFN-gamma and TGF-beta 1 were also shown in patients with AD. These results indicated a similarity (decreased levels of IFN-gamma and TGF-beta 1) between AD and AA based on the cytokine profile. In addition, decreased levels of IL-4 mRNA in AA might also explain the experience that the severity of atopic disease coincident with AA is mild in the most of cases. Next, we compared the levels of these cytokine mRNA among the three subgroups of AA that were categorized based on the severity of the symptoms: mild, severe and totalis. Although there was no significant difference between any combinations of the subgroups, there was a tendency to increase the levels of IFN-gamma mRNA and to decrease the levels of IL-4 mRNA according to the severity of alopecia. However, the levels of IFN-gamma mRNA in any subgroups were less than those of HC. These results suggest that IFN-gamma is therefore involved in the pathogenesis of AA, although the information from PBMC is limited. In conclusion, AA might be induced by an aberrant expression of IFN-gamma in individuals whose PBMC produce low amounts of IFN-gamma and TGF-beta 1. Further analysis is therefore required to investigate the phenotypes of the population in PBMC with or without reference to regulatory T cells.