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首页> 外文期刊>Journal of dermatological science >Specific substance of Maruyama (SSM) suppresses immune responses in atopic dermatitis-like skin lesions in DS-Nh mice by modulating dendritic cell functions.
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Specific substance of Maruyama (SSM) suppresses immune responses in atopic dermatitis-like skin lesions in DS-Nh mice by modulating dendritic cell functions.

机译：丸山的特定物质（SSM）通过调节树突状细胞功能来抑制DS-Nh小鼠特应性皮炎样皮肤病变中的免疫反应。

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BACKGROUND: Specific substance of Maruyama (SSM) is a carcinostatic immunotherapeutic agent extracted from Mycobacterium tuberculosis. The efficacy of SSM induced interleukin(IL)-12 and IFN-gamma production, and inhibition of IL-4, resulting in a shift from Th2 to Th1 in vivo. OBJECTIVE: The DS-Nh mice are a model of human atopic dermatitis (AD), which spontaneously develop dermatitis under conventional conditions. In this study, to determine whether SSM can prevent the development of skin lesions in a murine model of AD. METHODS: DS-Nh mice were injected with SSM 5 days per week for 11 weeks. Pharmacological, histological and serological studies were performed to investigate the therapeutic effect of SSM for DS-Nh mice. Analysis of cytokines responses to SSM using quantitative RT-PCR and flow cytometry were also performed to evaluate their therapeutic mechanisms in these AD model mice. RESULTS: Clinically, erythema, erosions, excoriation, and edema were observed in DS-Nh mice at 16 weeks of age, which advanced with age. Histologically, the relative number of mast cells increased in DS-Nh mice. SSM treatment alleviated the clinical and histological findings in accord with reduced serum IgE level, and increased IgG2a level. TSLP expression was not induced, but IL-1beta, IL-12, IL-17A, and IFN-gamma were induced in SSM-treated DS-Nh mice. Overall, SSM treatments increased the number of activated DCs in lesions. SSM induced CD80, CD86, and MHC class II expression on bone marrow-derived DCs. CONCLUSIONS: SSM enhanced IL-12 production, but suppressed TSLP expression, resulting in a shift from Th2 to Th1 responses. This shift suppressed AD-like skin lesions in a similar fashion as the BCG vaccine. Therefore, SSM may be a useful adjuvant for suppressing skin lesions in AD models.
机译：背景：丸山的特定物质（SSM）是从结核分枝杆菌提取的抗癌免疫治疗剂。 SSM的功效诱导了白介素（IL）-12和IFN-γ的产生，以及对IL-4的抑制，从而导致体内Th2转变为Th1。目的：DS-Nh小鼠是人类特应性皮炎（AD）的模型，它在常规条件下自发发展为皮炎。在这项研究中，确定SSM是否可以预防AD鼠模型中皮肤病变的发展。方法：DS-Nh小鼠每周5天注射SSM，共11周。进行了药理，组织学和血清学研究，以研究SSM对DS-Nh小鼠的治疗作用。还使用定量RT-PCR和流式细胞仪分析了对SSM的细胞因子反应，以评估它们在这些AD模型小鼠中的治疗机制。结果：在临床上，在16周龄的DS-Nh小鼠中观察到红斑，糜烂，剥落和水肿，并随着年龄的增长而发展。组织学上，DS-Nh小鼠中肥大细胞的相对数量增加。 SSM治疗减轻了血清IgE水平并增加了IgG2a水平，从而减轻了临床和组织学检查结果。未诱导TSLP表达，但在SSM处理的DS-Nh小鼠中诱导了IL-1beta，IL-12，IL-17A和IFN-γ。总体而言，SSM治疗增加了病变中激活的DC的数量。 SSM诱导源自骨髓的DC上的CD80，CD86和MHC II类表达。结论：SSM增强了IL-12的产生，但抑制了TSLP的表达，从而导致了从Th2反应向Th1反应的转变。这种转变以与BCG疫苗类似的方式抑制了AD样皮肤损伤。因此，SSM可能是抑制AD模型皮肤损伤的有用佐剂。

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