Diseases categorized as autoinflammatory keratinization diseases (AiKDs), and their pathologies and treatments.

毛发红糠疹 皮肤病科 医学 银屑病 免疫学
作者
Masashi Akiyama
出处
期刊:PubMed 卷期号:86 (1): 1-15
标识
DOI:10.18999/nagjms.86.1.1
摘要

Whole-exome and whole-genome sequencing have become widespread in approximately the last 15 years, and the predisposing factors and pathomechanisms of inflammatory keratinization diseases, which have been unknown for a long time, have gradually been revealed. Hence, various inflammatory keratinization diseases are recognized to cause innate immunity hyperactivation. Therefore, we have been advocating for the clinical entity, "autoinflammatory keratinization diseases (AiKDs)" since 2017. AiKDs are inflammatory keratinization diseases caused by autoinflammatory-related pathomechanisms in the skin. The aberrant activation of innate immunity and the resultant autoinflammation in the epidermis and the superficial dermis in AiKDs cause hyperkeratosis in the epidermis. Our initially proposed concept of AiKDs included generalized pustular psoriasis and related conditions, pityriasis rubra pilaris type V, and familial keratosis lichenoides chronica. Since then, the number of diseases known to be AiKDs has increased as previously unknown disease-causing factors and pathogenetic mechanisms of inflammatory keratinization diseases have been clarified one by one. To date, porokeratosis, hidradenitis suppurative, keratosis linearis with ichthyosis congenita and sclerosing keratoderma (KLICK) syndrome, and AiKDs associated with epidermal growth factor receptor (EGFR) deficiency or with hepatitis and autism have been recognized as AiKDs. The concept of AiKDs is considered extremely useful in our precise understanding of the pathogeneses behind inflammatory keratinization diseases and our appropriate treatment method selection. The number of AiKDs is expected to grow with the clarification of the pathomechanisms of further inflammatory keratinization diseases.
最长约 10秒,即可获得该文献文件

科研通智能强力驱动
Strongly Powered by AbleSci AI
更新
PDF的下载单位、IP信息已删除 (2025-6-4)

科研通是完全免费的文献互助平台,具备全网最快的应助速度,最高的求助完成率。 对每一个文献求助,科研通都将尽心尽力,给求助人一个满意的交代。
实时播报
刚刚
浮游应助kuankuan采纳,获得10
1秒前
Abner发布了新的文献求助10
1秒前
blackyu发布了新的文献求助10
3秒前
So发布了新的文献求助10
3秒前
心灵美天奇完成签到 ,获得积分10
3秒前
紫紫发布了新的文献求助10
4秒前
香蕉觅云应助小池采纳,获得10
4秒前
4秒前
5秒前
十七发布了新的文献求助10
5秒前
5秒前
6秒前
齐佳完成签到,获得积分10
6秒前
6秒前
早爹发布了新的文献求助10
7秒前
kai150333429发布了新的文献求助10
8秒前
8秒前
xppxhn完成签到,获得积分10
8秒前
8秒前
wanglong0118发布了新的文献求助10
9秒前
慈祥的蛋挞完成签到,获得积分10
9秒前
左友铭发布了新的文献求助10
9秒前
人生何处不相逢完成签到,获得积分10
10秒前
123456发布了新的文献求助10
11秒前
天天快乐应助Stone采纳,获得10
12秒前
浮游应助wanglong0118采纳,获得10
12秒前
深情安青应助紫紫采纳,获得10
13秒前
bkagyin应助Mia采纳,获得10
13秒前
buhuidanhuixue完成签到,获得积分10
13秒前
啊啊啊哦哦哦完成签到,获得积分10
13秒前
ggctxh发布了新的文献求助10
13秒前
14秒前
14秒前
枯藤老柳树完成签到,获得积分10
14秒前
研友_VZG7GZ应助大号安全蛋采纳,获得10
14秒前
Larry1226发布了新的文献求助10
14秒前
开始啦完成签到,获得积分10
16秒前
科研通AI2S应助So采纳,获得10
16秒前
超级安荷完成签到,获得积分10
17秒前
高分求助中
(应助此贴封号)【重要!!请各用户(尤其是新用户)详细阅读】【科研通的精品贴汇总】 10000
Bandwidth Choice for Bias Estimators in Dynamic Nonlinear Panel Models 2000
HIGH DYNAMIC RANGE CMOS IMAGE SENSORS FOR LOW LIGHT APPLICATIONS 1500
茶艺师试题库(初级、中级、高级、技师、高级技师) 1000
Constitutional and Administrative Law 1000
The Social Work Ethics Casebook: Cases and Commentary (revised 2nd ed.). Frederic G. Reamer 800
Vertebrate Palaeontology, 5th Edition 570
热门求助领域 (近24小时)
化学 材料科学 医学 生物 工程类 有机化学 生物化学 物理 纳米技术 计算机科学 内科学 化学工程 复合材料 物理化学 基因 遗传学 催化作用 冶金 量子力学 光电子学
热门帖子
关注 科研通微信公众号,转发送积分 5360761
求助须知:如何正确求助?哪些是违规求助? 4491279
关于积分的说明 13981825
捐赠科研通 4393949
什么是DOI,文献DOI怎么找? 2413668
邀请新用户注册赠送积分活动 1406502
关于科研通互助平台的介绍 1381004