Anti-interleukin 33 treatment alleviates psoriatic dermatitis in mice induced imiquimod

IF 5.6 2区 医学 Q2 IMMUNOLOGY
International immunopharmacology Pub Date : 2023-08-01 Epub Date: 2023-06-19 DOI:10.1016/j.intimp.2023.110480
Dandan Fu , Shuting Zheng , Jialin Li , Hua Hu , Qingqing Wang , Xiuyu Fu , Min Li , Dong Yan , Zishan Yang , Zhongwei Tian , Xiangfeng Song
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Abstract

Interleukin-33(IL-33), is constitutively expressed in the epithelial cells of the skin. It has been reported that IL-33 contributed to the severity of the disease in psoriasis-like mouse models. In the current study, we evaluated the effect of anti-IL-33 antibody (Ab) in imiquimod-induced psoriatic dermatitis in mice. Our observations showed that anti-IL-33 Ab ameliorated the erythema, scaling, epidermal thickness and spleen index. Additionally, we found anti-IL-33 Ab significantly decreased the expression of psoriasis-related cytokines. Moreover, anti-IL-33 Ab significantly reduced Ki-67 positive cells, CD3+CD4+T cells, and CD3+CD8+T cells in the skin lesions. Furthermore, anti-IL-33 Ab treatment down-regulated the expression of phosphorylation of STAT3 and IL-33 in model mouse. These results indicated that the anti-IL-33 Ab alleviated the seriousness of skin lesions, inhibited the activation of the STAT3, lymphocyte infiltration and the secretion of pro-inflammatory cytokines in imiquimod-induced psoriatic dermatitis in mice, suggesting IL-33 may be a therapeutic target for the treatment of psoriasis.

抗白细胞介素33治疗可减轻咪喹莫特所致小鼠银屑病皮炎
白细胞介素-33(IL-33)在皮肤上皮细胞中组成性表达。据报道,IL-33在牛皮癣样小鼠模型中有助于疾病的严重程度。在本研究中,我们评估了抗il -33抗体(Ab)在吡喹莫德诱导的银屑病皮炎小鼠中的作用。我们的观察显示,抗il -33 Ab改善了红斑、鳞屑、表皮厚度和脾脏指数。此外,我们发现抗il -33 Ab显著降低银屑病相关细胞因子的表达。此外,抗il -33 Ab显著降低皮肤病变中Ki-67阳性细胞、CD3+CD4+T细胞和CD3+CD8+T细胞。此外,抗IL-33 Ab处理可下调模型小鼠STAT3和IL-33磷酸化表达。这些结果表明,抗IL-33 Ab减轻了吡喹莫特诱导的银屑病皮炎小鼠皮损的严重程度,抑制了STAT3的激活、淋巴细胞的浸润和促炎细胞因子的分泌,提示IL-33可能是治疗银屑病的治疗靶点。
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来源期刊
CiteScore
8.40
自引率
3.60%
发文量
935
审稿时长
53 days
期刊介绍: International Immunopharmacology is the primary vehicle for the publication of original research papers pertinent to the overlapping areas of immunology, pharmacology, cytokine biology, immunotherapy, immunopathology and immunotoxicology. Review articles that encompass these subjects are also welcome. The subject material appropriate for submission includes: • Clinical studies employing immunotherapy of any type including the use of: bacterial and chemical agents; thymic hormones, interferon, lymphokines, etc., in transplantation and diseases such as cancer, immunodeficiency, chronic infection and allergic, inflammatory or autoimmune disorders. • Studies on the mechanisms of action of these agents for specific parameters of immune competence as well as the overall clinical state. • Pre-clinical animal studies and in vitro studies on mechanisms of action with immunopotentiators, immunomodulators, immunoadjuvants and other pharmacological agents active on cells participating in immune or allergic responses. • Pharmacological compounds, microbial products and toxicological agents that affect the lymphoid system, and their mechanisms of action. • Agents that activate genes or modify transcription and translation within the immune response. • Substances activated, generated, or released through immunologic or related pathways that are pharmacologically active. • Production, function and regulation of cytokines and their receptors. • Classical pharmacological studies on the effects of chemokines and bioactive factors released during immunological reactions.
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