分子系统过程和细胞机制——引起特应性皮炎皮肤状况的瘙痒、刺痛和疼痛及其对创新治疗的影响

V. R. Raju
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摘要

特应性皮炎(AD)是一种长期煽动性、群众性和炎症性皮肤疾病。受试者(即患者)通过特应性皮炎遭受与极度瘙痒和不适相关的燃烧性病变,这导致睡眠障碍(也很少有呼吸暂停),精神和心理健康状况不佳,生活质量(QoL)也很差。本研究探讨了特应性皮炎中引起瘙痒、刺痛、刺激和疼痛症状的分子系统过程/机制,并探讨了目前轻度至急性特应性皮炎治疗的临床和医学进展。AD的分子病理包含异常的免疫、保护性刺激,包括皮肤、安全细胞和神经细胞/神经元细胞之间的大量交叉对话。外源性和内源性触发因素调节皮肤和免疫细胞对包括细胞因子/趋化因子表达/释放在内的介质的刺激,从而引起炎症、皮肤屏障破坏、感觉神经元的激活和生长、瘙痒和疼痛。细胞类型之间这些复杂的相互作用主要由细胞因子介导,但也涉及趋化因子、神经递质、脂质、蛋白酶、抗菌肽、离子通道激动剂或各种G蛋白偶联受体。:特应性皮炎患者具有以白细胞介素4、12、13、18、22、31和33水平异常为特征的细胞因子谱;胸腺基质淋巴生成素;还有干扰素。细胞因子受体主要通过Janus激酶/信号转导器和转录途径的激活器发出信号。在新兴的新疗法中,几种Janus激酶抑制剂正被开发用于局部或(一般或全身)系统治疗轻度到急性AD炎,因为它们有能力调节细胞因子的变化,然后可用。Janus-kinase阻碍导致基因表达的变化,这对局部和一般(普遍)细胞因子释放有积极影响,可能还有额外的中介,因此很好地调节了AD患者的刺激、瘙痒、刺痛和疼痛的分子细胞机制。这项研究探讨了皮肤出现粉红色、发炎和伤口的皮肤病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Molecular systems processes and cellular mechanisms-causing to itching tingling and aching in atopic dermatitis skin conditions and repercussions for innovative therapeutics
: Atopic dermatitis (AD) is a prolonged seditious, rabble rousing, and inflammatory—provocative skin disease. The subjects (i.e., patients) by means of atopic-dermatitis suffer incendiary lesions linked through extreme itching plus discomfort, and that is leading to sleep disorder (and also rarely apnea), weak mental and psychological health and also quality-of-life (QoL). : This study discusses the molecular systems processes/mechanisms causing to itching, tingling and irritation plus aching signs in atopic-dermatitis and examine the existing clinical, medical-advancement of therapies for mild-to-acute atopic-dermatitis. : The molecular pathology of AD contains abnormal immune, protected stimulation including substantial crisscross-talk amongst the skin and safe and neural cells/neuronal cells. Exogenous and endogenous triggers modulate stimulus of mediators including cytokine/chemokine expression/release by the skin and immune cells, which causes inflammation, skin barrier disruption, activation and growth of sensory neurons, itching and paining. These complex interactions among cell types are mediated primarily by cytokines, but also involve chemokines, neurotransmitters, lipids, proteases, antimicrobial peptides, and agonists of ion channels or various G protein–coupled receptors. : Patients with atopic dermatitis have a cytokine profile characterized by abnormal levels of interleukins 4,12,13,18,22,31 and 33; thymic stromal lymphopoietin; and interferon gamma. Cytokine receptors mainly signal through the Janus kinase/signal transducer and activator of transcription pathways. Among emerging novel therapeutics, several Janus kinase inhibitors are being developed for topical or (general nut systemic) systematic treatment of mild to acute AD tis as of their ability to regulate-cytokine countenance then make available. Janus-kinase hampers take the lead to variations in genetic representation which has positive impacts on provincial and general (universal) cytokine-release, and possibly additional intermediaries, so well regulating molecular-cellular-mechanisms accountable for irritation, itching, tingling followed by agony in AD. : This study explored the skin disorder in which the skin develops pink, inflamed plus wound.
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