Therapeutic New Era for Atopic Dermatitis: Part 1. Biologics.

Therapeutic New Era for Atopic Dermatitis: Part 1. Biologics.
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特应性皮炎的治疗新时代:第1部分。生物制剂。

DOI:
10.5021/ad.2021.33.1.1
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发表时间:
2021-03
影响因子:
1.6
通讯作者:
Simpson EL
Simpson EL
中科院分区:
医学4区
文献类型:
--
作者:
Ahn J;Choi Y;Simpson EL

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特应性皮炎(AD)是一种由免疫失调和皮肤屏障功能障碍引起的慢性炎症性皮肤疾病。我们目前正在经历一个了解AD发病机制的新时代,因此,一个治疗创新的新时代,包括小分子和生物治疗。近年来,转化研究的进展已经挑战了传统的AD发病机制范式,即AD仅仅是一种Th 2-显性疾病。其他免疫途径似乎在复杂的AD病理生理学中发挥作用,尽管这些额外的免疫途径异常的临床相关性尚不清楚。1型、22型和17型通路激活(与相关细胞因子/趋化因子)已在AD患者的皮肤和血液中得到证实。AD急性病变中2型(白细胞介素[IL]-4,IL-13)、IL-31和22型(IL-22)途径细胞因子增加。IL-22诱导急性AD发作时的表皮增生和终末分化S100基因的显著增加。这种对发病机制的理解与AD治疗发展的历史性增长相对应。AD的极端临床异质性和慢性进展需要更新,更安全,更有效的治疗方法,控制疾病,改善患者的生活质量。
Atopic dermatitis (AD) is a chronic, inflammatory cutaneous disease driven by immune dysregulation and skin barrier dysfunction. We are currently experiencing a new era of understanding of the pathogenesis of AD and, as a consequence, a new era of innovation in therapeutics, including small molecules and biologic therapy. Recently, advances in translational research have challenged the traditional AD pathogenesis paradigm of AD being solely a Th2-dominant disease. Other immune pathways seem to play a role in the complex AD pathophysiology, although the clinical relevance of these additional immune pathway abnormalities is unclear. Type 1, type 22, and type 17 pathway activation (with related cytokines/chemokines) have been demonstrated in the skin and blood of AD patients. Type 2 (interleukin [IL]-4, IL-13), IL-31, and type 22 (IL-22) pathway cytokines are increased in AD acute lesions. IL-22 induces both an epidermal hyperplasia at the onset of acute AD and a marked increase in the terminal differentiation S100 genes. This understanding of pathogenesis corresponds to a historic increase in therapeutic development in AD. The extreme clinical heterogeneity and the chronic progression of AD establish the need for newer, safer, and more effective treatments, control the disease, and improve the quality of life of affected patients.
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