化脓性汗腺炎是一种发生在腋窝、腹股沟、臀部、肛周等皮肤褶皱部位的慢性复发性炎症性皮肤病.该病好发于年轻女性,主要的临床表现为疼痛性炎性结节、脓肿、破溃以及窦道和瘢痕形成.该病病程长且反复发作,严重影响患者的生活质量.化脓性汗腺炎还可与其他代谢性疾病或心血管疾病并发,缩短患者的寿命.化脓性汗腺炎的确切发病机制目前仍不清楚,学术界认为包括遗传因素在内的多种因素起综合的致病作用.目前化脓性汗腺炎的治疗手段限于抗感染以及其他对症治疗措施,故而治疗效果有限.现主流观点认为异常激活的免疫系统,包括异常升高的TNF-α、IL-17、IL-12、IL-23等细胞因子,可能在其发病过程中发挥着重要作用.随着对化脓性汗腺炎病理生理过程的了解,以及对于并发其他炎症性疾病的患者进行生物治疗有效性的观察,对化脓性汗腺炎的生物治疗获得了广泛的关注.基于多项临床试验的结果,美国FDA批准了抗TNF-α单克隆抗体阿达木单抗作为治疗化脓性汗腺炎的唯一生物制剂.同时,以上述炎症细胞因子为靶标的其他生物制剂也在中重度化脓性汗腺炎的治疗中显示了良好的疗效和安全性.本文在简单介绍化脓性汗腺炎的基础上,主要对化脓性汗腺炎所涉及的免疫因子的靶向生物治疗进展作一综述.

瘙瘁是银屑病患者常见的临床症状,易造成患者的痛苦,降低患者生活质量.除神经系统、免疫系统、血管系统以及皮肤之间的相互作用外,其他相关因子也可能参与了银屑病瘙痒机制.深入探索银屑病瘙痒机制,能为银屑病瘙瘁的治疗提供新的思路和方法,从而更加针对性地治疗银屑病患者的瘙痒症状.

Objective:To evaluate the proliferative activity of and changes in the expression of related differentiation proteins in a stably NCSTN gene-silenced human immortalized keratinocyte cell line HaCaT, and to preliminarily explore the possible mechanism underlying the occurrence of acne inversa.Methods:By lentivirus-mediated short hairpin RNA (shRNA) , a NCSTN gene-silenced HaCaT cell model was established (shRNA group) , and other HaCaT cells transfected with empty lentivirus served as a negative control group. Real-time quantitative PCR and Western blot analysis were performed to determine the NCSTN gene-silencing efficiency. Cell counting kit-8 (CCK8) assay was conducted to evaluate the proliferative activity of HaCaT cells, and real-time quantitative PCR and Western blot analysis were performed to determine the mRNA and protein expression of cytokeratins (CK1, CK5, CK7, CK10, CK14, CK16, CK17, CK18, CK19 and CK20) and other differentiation molecules (involucrin and loricrin) respectively in HaCaT cells. Two-independent-sample t test was used to compare the measurement data between two groups. Results:NCSTN mRNA and protein expression were significantly lower in the shRNA group (0.42 ± 0.19, 0.30 ± 0.07 respectively) than in the negative control group (1.00 ± 0.34, 1.00 ± 0.26; t = 5.196, 2.637, P < 0.001, < 0.05, respectively) , and the gene-silencing efficiency was 70%. Compared with the negative control group, the shRNA group showed higher cellular proliferative activity, but decreased protein expression of CK16, CK19 and terminal differentiation molecule involucrin ( t = 3.787, 3.817, 2.904, P < 0.01, < 0.05, < 0.05, respectively) . Conclusion:Stable silencing of NCSTN gene can lead to abnormal proliferation and differentiation of HaCaT cells, which provides new ideas for subsequent exploration of acne inversa caused by NCSTN gene mutation.