Abstract：
UNASSIGNED: IL-36 cytokines are members of the IL-1 superfamily. Increasing evidence in the IL-36 pathway demonstrates their potential as a therapeutic target for treating inflammatory skin diseases, such as generalized pustular psoriasis (GPP).
UNASSIGNED: A narrative review was written to further study preclinical and clinical evidence for the role of IL-36 in psoriasis, atopic dermatitis (AD), hidradenitis suppurativa (HS), acne, autoimmune blistering diseases, and neutrophilic dermatoses.
UNASSIGNED: IL-36 has important downstream effects such as inducing expression of inflammatory cytokines, antimicrobial peptides, and growth factors. Increased expression of IL-36 cytokines has been observed in the lesional skin of patients with psoriasis. Studies of other inflammatory skin diseases have also noted similar findings, albeit to a lesser extent. IL-36 inhibition has been shown to be effective in GPP and is currently being studied for other inflammatory skin diseases.
UNASSIGNED: The IL-36 pathway contributes to pathogenesis of many inflammatory skin diseases and is a promising therapeutic target.
UNASSIGNED: A narrative review was written to further study preclinical and clinical evidence for the role of IL-36 in psoriasis, atopic dermatitis (AD), hidradenitis suppurativa (HS), acne, autoimmune blistering diseases, and neutrophilic dermatoses.
UNASSIGNED: IL-36 has important downstream effects such as inducing expression of inflammatory cytokines, antimicrobial peptides, and growth factors. Increased expression of IL-36 cytokines has been observed in the lesional skin of patients with psoriasis. Studies of other inflammatory skin diseases have also noted similar findings, albeit to a lesser extent. IL-36 inhibition has been shown to be effective in GPP and is currently being studied for other inflammatory skin diseases.
UNASSIGNED: The IL-36 pathway contributes to pathogenesis of many inflammatory skin diseases and is a promising therapeutic target.
摘要：
未经批准:IL-36细胞因子是IL-1超家族的成员。在IL-36途径中越来越多的证据证明了它们作为治疗炎症性皮肤病的治疗靶点的潜力。如全身性脓疱型银屑病（3GPP）。
UASSIGNED：撰写了叙述性综述，以进一步研究IL-36在银屑病中的作用的临床前和临床证据，特应性皮炎(AD),化脓性汗腺炎（HS），痤疮,自身免疫性起泡疾病，和嗜中性皮肤病。
未经证实：IL-36具有重要的下游作用，如诱导炎症细胞因子的表达，抗菌肽，和增长因素。已在牛皮癣患者的皮损中观察到IL-36细胞因子的表达增加。其他炎症性皮肤病的研究也注意到类似的发现，虽然程度较小。IL-36抑制已被证明是有效的，目前正在研究其他炎症性皮肤病。
未经证实：IL-36途径与许多炎症性皮肤病的发病机制有关，是一个有前途的治疗靶点。
UASSIGNED：撰写了叙述性综述，以进一步研究IL-36在银屑病中的作用的临床前和临床证据，特应性皮炎(AD),化脓性汗腺炎（HS），痤疮,自身免疫性起泡疾病，和嗜中性皮肤病。
未经证实：IL-36具有重要的下游作用，如诱导炎症细胞因子的表达，抗菌肽，和增长因素。已在牛皮癣患者的皮损中观察到IL-36细胞因子的表达增加。其他炎症性皮肤病的研究也注意到类似的发现，虽然程度较小。IL-36抑制已被证明是有效的，目前正在研究其他炎症性皮肤病。
未经证实：IL-36途径与许多炎症性皮肤病的发病机制有关，是一个有前途的治疗靶点。
