Agelopoulos Konstantin, Wiegmann Henning, Schmelz Martin, Ständer Sonja
Kompetenzzentrum chronischer Pruritus, Universitätsklinikum Münster, Albert-Schweitzer-Campus 1, 48149, Münster, Deutschland.
Abteilung Experimentelle Schmerzforschung, CBTM, Med. Fakultät Mannheim, Universität Heidelberg, Mannheim, Deutschland.
Dermatologie (Heidelb). 2022 Aug;73(8):593-599. doi: 10.1007/s00105-022-05017-1. Epub 2022 Jun 13.
The underlying mechanisms of pruritus and chronic pruritus (CP) in particular, remain poorly understood; however, current research has revealed promising new concepts in which the importance of the interaction of neuronal cells of different classes, immune cells and keratinocytes is becoming increasingly clearer.
In this review article the current concepts in pruritus research are presented and summarized.
This is a review article based on the current literature.
Different classes of sensory afferents, such as mechano-insensitive C‑fibers (histaminergic pruritus) and non-histaminergic pruriceptive C‑fibers and Aδ-fibers are involved in CP. The central sensitization in CP manifests as hyperknesis and alloknesis, the latter triggered by Aβ-fibers and Merkel cells. In recent years, the importance of inflammatory cells, such as Th1 and Th2 cells but also basophilic, eosinophilic granulocytes and mast cells has become clear. In CP there appears to be close communication between neuronal cells, immune cells and keratinocytes. Recent studies have focused on proinflammatory interleukins, such as IL-31, IL‑4 and IL-13 and their receptors. The Janus kinase/signal transducers and activators of transcription (JAK/STAT) signaling pathway also plays an important role in the triggered signaling cascades that ultimately lead to pruritus perception. Therefore, in current treatment studies not only the interleukins and their receptors but also the JAK/STAT signaling pathway are directly targeted.
The discovery of new mechanisms and interactions in CP highlights the complexity of this disease. Even if this and the treatment options derived from this are already very promising, a much better understanding of the mechanisms of CP is urgently needed in order to enable further options for an optimized treatment.
瘙痒尤其是慢性瘙痒（CP）的潜在机制仍未得到充分理解；然而，目前的研究已经揭示了一些有前景的新概念，其中不同类型的神经元细胞、免疫细胞和角质形成细胞之间相互作用的重要性日益明晰。
在这篇综述文章中，将对瘙痒研究的当前概念进行呈现和总结。
这是一篇基于当前文献的综述文章。
不同类型的感觉传入神经，如机械不敏感的C纤维（组胺能性瘙痒）、非组胺能性瘙痒感受性C纤维和Aδ纤维都参与了慢性瘙痒。慢性瘙痒中的中枢敏化表现为运动亢进和异常性疼痛，后者由Aβ纤维和默克尔细胞触发。近年来，炎症细胞，如Th1和Th2细胞以及嗜碱性粒细胞、嗜酸性粒细胞和肥大细胞的重要性已变得清晰。在慢性瘙痒中，神经元细胞、免疫细胞和角质形成细胞之间似乎存在密切的通讯。最近的研究集中在促炎细胞因子，如IL-31、IL-4和IL-13及其受体。Janus激酶/信号转导子和转录激活子（JAK/STAT）信号通路在最终导致瘙痒感知的触发信号级联反应中也起着重要作用。因此，在当前的治疗研究中，不仅细胞因子及其受体，而且JAK/STAT信号通路都被直接作为靶点。
慢性瘙痒中新机制和相互作用的发现凸显了这种疾病的复杂性。即使这一点以及由此衍生的治疗选择已经非常有前景，但仍迫切需要更好地理解慢性瘙痒的机制，以便能够有进一步优化治疗的选择。
