搔癢是皮膚科患者求診的最常見主訴，並會嚴重影響患者損害生活品質。搔癢是經由發炎性介質、神經傳遞物質和神經胜肽等，刺激活化皮膚神經末梢，導致搔癢信號從周邊皮膚通過脊髓，再傳遞到大腦皮層。雖然一些發炎性皮膚病，如紅斑狼瘡、蜂窩組織炎和苔蘚樣糠疹，可能不太會引起或只有輕微搔癢，但牛皮癬和異位性皮膚炎等其他發炎性皮膚病，會在大多數患者中引起中度至重度搔癢。因此探查導致這種差異的關鍵介質對於搔癢的傳導非常重要。另外非發炎性皮膚疾病，如尿毒症搔癢，通過皮膚中的某些搔癢原引起搔癢，卻沒有皮膚的發炎皮膚變化。同時，有證據表明，搔癢原不僅會引起搔癢，還會與免疫細胞相互作用並充當發炎介質，從而加劇疾病活性。所以能夠增加對這些媒介物以及發炎性和非發炎性致癢原的了解，能有效就常見的搔癢性皮膚病建立目標性治療。

Itch is the main chief complaint in patients visiting dermatologic clinics and has the ability to deeply impair life quality. Itch results from activation of cutaneous nerve endings by noxious stimuli such as inflammatory mediators, neurotransmitters and neuropeptides, causing itch signal transduction from peripheral skin, through the spinal cord and thalamus, to the brain cortex. While some inflammatory skin diseases such as lupus erythematosus, cellulitis, and pityriasis lichenoides may or may not cause itch, others such as psoriasis and atopic dermatitis cause moderate-to-severe itch in a majority of the patients. It is important to find the key mediators that cause such differences. On the other hand, primarily noninflammatory diseases, such as uremic pruritus, cause itch through certain pruritogens without causing skin inflammatory change. Meanwhile, there is evidence that pruritogens are not only responsible for eliciting pruritus, but also interact with immune cells and act as inflammatory mediators, which exacerbate disease activities. The understanding of these mediators can provide targeted therapies for inflammatory and noninflammatory itch in common itching skin diseases.