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What causes itch in atopic dermatitis?

机译:什么原因导致特应性皮炎瘙痒?

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Itch, the hallmark of atopic dermatitis, has a significant impact on quality of life for patients with this disease. Various central and peripheral mediators have been suggested to play a role in the pathophysiology of atopic eczema itch. Significant cross-talk occurs among stratum corneum, keratinocytes, immune cells, and nerve fibers, which are in close proximity to one another and induce itch. The impaired barrier function associated with the itch-scratch cycle further augments this vicious cycle. Recent advances in our understanding of itch pathophysiology shed light on peripheral and central neural sensitization of nerve fibers that contribute significantly to itch in atopic dermatitis. Recently, several new mediators have been described as associated with itch in atopic dermatitis, including serine proteases, interleukin 31, and nerve growth factor. This review covers the peripheral and central mechanisms and mediators involved in pathogenesis of itch in atopic dermatitis.
机译:瘙痒是特应性皮炎的标志,对这种疾病患者的生活质量有重大影响。已经提出了各种中枢和外周介质在特应性湿疹瘙痒的病理生理中起作用。在角质层,角质形成细胞,免疫细胞和神经纤维之间会发生严重的串扰,它们彼此非常接近并会引起瘙痒。与瘙痒-抓痒循环相关的屏障功能受损进一步加剧了这种恶性循环。我们对瘙痒病理生理学的了解的最新进展为神经纤维的周围和中枢神经敏化提供了启示,这些神经纤维对特应性皮炎中的瘙痒有重大贡献。最近,已经描述了几种与特应性皮炎瘙痒有关的新介体,包括丝氨酸蛋白酶,白介素31和神经生长因子。这篇综述涵盖了特应性皮炎瘙痒发病机理的外周和中枢机制及介体。

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