Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Department of Dermatology and Plastic Surgery, Akita University Graduate School of Medicine, Akita, Japan.
Australas J Dermatol. 2020 Feb;61(1):e39-e45. doi: 10.1111/ajd.13143. Epub 2019 Aug 19.
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).
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.
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.
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.
白细胞介素（IL）-36 家族成员，IL-36α、IL-36β 和 IL-36γ，是对中性粒细胞和嗜酸性粒细胞具有强烈趋化作用的细胞因子。IL-36 受体拮抗剂（IL-36Ra）抑制 IL-36α、IL-36β 和 IL-36γ 的活性。然而，IL-36α、IL-36β、IL-36γ 和 IL-36Ra 的免疫组织化学表达在正常滤泡、滤泡炎或嗜酸性脓疱性毛囊炎（EPF）中从未被提及过。
我们使用 10 例 EPF、9 例非特异性滤泡炎、10 例正常皮肤样本和 10 例皮脂腺痣旁正常滤泡样本进行了 IL-36α、IL-36β、IL-36γ 和 IL-36Ra 的免疫组织化学染色。两位皮肤科医生对所有切片进行了盲法评估，他们不了解患者的病历。
在正常皮肤、滤泡炎或 EPF 中，几乎无法检测到有活性的 IL-36α 在滤泡上皮和表皮中的表达。与正常滤泡相比，IL-36β、IL-36γ 和 IL-36Ra 的表达在滤泡炎和 EPF 中均增加。在正常滤泡中，IL-36β 与 IL-36Ra 之间、IL-36γ 与 IL-36Ra 之间存在负相关关系；然而，在滤泡炎中，这种关系不存在。与正常滤泡和滤泡炎相反，在 EPF 中，IL-36β/γ 与 IL-36Ra 之间存在显著的正相关关系。
IL-36β、IL-36γ 和 IL-36Ra 的过度表达是滤泡炎和 EPF 炎症反应的一个组成部分。IL-36γ 和 IL-36Ra 的协调表达可能与 EPF 的发病机制有关。
