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首页> 外文期刊>The Australasian journal of dermatology >Upregulation of IL IL ‐36 cytokines in folliculitis and eosinophilic pustular folliculitis
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Upregulation of IL IL ‐36 cytokines in folliculitis and eosinophilic pustular folliculitis

机译:UL IL -36细胞因子在毛囊炎和嗜酸性脓疱疮性毛囊炎的上调

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摘要

Abstract Background Members of the interleukin ( IL )‐36 family, IL ‐36α, IL ‐36β and IL ‐36γ, are potent chemoattractive cytokines for neutrophils and eosinophils. IL ‐36 receptor antagonist ( IL ‐36Ra) inhibits IL ‐36α, IL ‐36β and IL ‐36γ activity. However, the immunohistological expression of IL ‐36α, IL ‐36β, IL ‐36γ and IL ‐36Ra has never been addressed in normal follicles, folliculitis or eosinophilic pustular folliculitis ( EPF ). Methods We performed immunohistochemical staining for IL ‐36α, IL ‐36β, IL ‐36γ and IL ‐36Ra using 10 cases of EPF , nine of non‐specific folliculitis, 10 normal skin samples and 10 samples of normal follicles adjacent to a sebaceous naevus as a control. Two dermatologists, who were blind to the patient records, evaluated all of the slides. Results The immunoreactive IL ‐36α was hardly detected in the follicular epithelium and epidermis in the normal skin, folliculitis or EPF . The expression of IL ‐36β, IL ‐36γ and IL ‐36Ra was augmented in both folliculitis and EPF compared with that in normal follicles. Negative correlations were detected between IL ‐36β and IL ‐36Ra and between IL ‐36γ and IL ‐36Ra in normal follicles; however, these were absent in folliculitis. In contrast to normal follicles and folliculitis, a significant positive correlation between IL ‐36β/γ and IL ‐36Ra was shown in EPF . Conclusions The overexpression of IL ‐36β, IL ‐36γ and IL ‐36Ra is an integral part of the inflammatory response of folliculitis and EPF . The coordinated expression of IL ‐36γ and IL ‐36Ra may be related to the pathomechanism of EPF .
机译:摘要白细胞介素(IL)-36系列,IL-36α,IL-36β和IL-36γ的背景构件是嗜中性粒细胞和嗜酸性粒细胞的有效化学性细胞因子。 IL -36受体拮抗剂(IL -36RA)抑制IL-36α,IL-36β和IL-36γ活性。然而,IL-36α,IL-36β,IL-36γ和IL-36RA的免疫组织表达从未在普通卵泡,毛囊炎或嗜酸性脓毒症毛囊炎(EPF)中得到解决。方法采用10例EPF,九种非特异性卵泡炎,10例正常皮肤样品和10例邻近皮脂钠的常规卵泡样品,对IL-36α,IL-36β,IL-36γ和IL -36RA进行免疫组化染色。控制。两位皮肤科医生对患者记录视而不见,评估了所有幻灯片。结果在正常的皮肤,毛囊炎或EPF中,在滤泡上皮和表皮中几乎没有检测到免疫反应性IL-36α。与正常卵泡相比,IL-36β,IL-36γ和IL -36RA的表达增强了毛囊炎和EPF。在IL-36β和IL-36RA之间检测到负相关性,在正常卵泡中的IL-36γ和IL -36RA之间;然而,这些在毛囊炎中不存在。与正常卵泡和卵泡炎相反,IL-36β/γ和IL -36RA之间的显着正相关在EPF中显示。结论IL-36β,IL-36γ和IL -36RA的过表达是毛囊炎和EPF的炎症反应的一部分。 IL-36γ和IL -36RA的协调表达可能与EPF的土程机制有关。

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