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首页> 外文期刊>Clinical and experimental allergy : >The development of atopic dermatitis is independent of Immunoglobulin E up-regulation in the K14-IL-4 SKH1 transgenic mouse model.
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The development of atopic dermatitis is independent of Immunoglobulin E up-regulation in the K14-IL-4 SKH1 transgenic mouse model.

机译：特应性皮炎的发展与K14-IL-4 SKH1转基因小鼠模型中的免疫球蛋白E上调无关。

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BACKGROUND: We have successfully generated an IgE-associated (extrinsic/allergic) mouse model of atopic dermatitis in K14-IL-4-Tg/CByB6 mice. The newly described subset of non-IgE-associated (intrinsic/non-allergic) atopic dermatitis in human patients raises the question on the role of IgE in the pathogenesis. OBJECTIVE: The aim of this study was to develop a non-IgE-associated atopic dermatitis model in K14-IL-4-Tg/SKH1 mice. METHODS: K14-IL-4-Tg/CByB6 mice were crossed with SKH1 mice to produce K14-IL-4-Tg/SKH1 mice. Phenotypes of clinical and histological, cytokine expression in the skin lesions, and total serum IgE in K14-IL-4-Tg/CByB6 and K14-IL-4-Tg/SKH1 mice were compared. The CD40 and CD40L on T and B cells were also studied to differentiate their roles in IgE production. RESULTS: K14-IL-4-Tg/SKH1mice had a normal total serum IgE level and manifested a chronic inflammatory skin phenotype identical to that of K14-IL-4-Tg/CByB6 IgE-mediated mice in clinical morphology, histology, infiltration of mononuclear cells/eosinophils/mast cells, mast cell degranulation, and up-regulation of chronic lesional cytokine mRNA expression of IL-1 beta, IL-3, IL-4, IL-6, IL-10, IL-12, IL-13, IFN-gamma, TNF-alpha, and TNF-beta. We also found that the inability of CD4(+) T cells of the K14-IL-4-Tg/SKH1mice to up-regulate CD40L expression upon stimulation might account for their inability to up-regulate the IgE level. B cell abnormality was ruled out as CD19(+) B cells of K14-IL-4-Tg/SKH1 mice synthesized the same amount of IgE in vitro compared with K14-IL-4-Tg/CByB6 mice in the presence of IL-4 and soluble CD40L. Our studies further suggested that the defect of early growth response-1 in T cells might be responsible for the impaired CD40L up-regulation in K14-IL-4-Tg/SKH1 mice. CONCLUSION: K14-IL-4-Tg/SKH1 mice developed skin inflammation that resembled human intrinsic atopic dermatitis. Therefore, this model may be suitable to study the pathogenesis of intrinsic atopic dermatitis.
机译：背景：我们已经成功地生成了K14-IL-4-TG / CByB6小鼠的IgE相关（外本/过敏性）小鼠模型。新描述的非IgE相关（内在/非过敏性）特应性皮炎中的人类患者的特征性皮炎提出了IgE在发病机制中的作用问题。目的：该研究的目的是在K14-IL-4-TG / SKH1小鼠中开发非IgE相关的特征性皮炎模型。方法：将K14-IL-4-TG / CBYB6小鼠与SKH1小鼠交叉以产生K14-IL-4-TG / SKH1小鼠。比较皮肤病变中临床和组织学，细胞因子表达的表型，以及K14-IL-4-TG / CBYB6和K14-IL-4-TG / SKH1小鼠中的总血清IgE。还研究了CD40和CD40L和B细胞的CD40L，以区分其在IgE产生中的作用。结果：K14-IL-4-TG / SKH1MICE具有正常的总血清IGE水平，表现出慢性炎症皮肤表型与K14-IL-4-TG / CBYB6 IGE介导的小鼠相同的临床形态，组织学，渗透单核细胞/嗜酸性粒细胞/肥大细胞，肥大细胞脱粒，慢性损伤细胞因子mRNA表达IL-1β，IL-3，IL-4，IL-6，IL-10，IL-12，IL-的慢性损伤细胞因子mRNA表达。 13，IFN-Gamma，TNF-α和TNF-β。我们还发现，K14-IL-4-TG / SKH1MICE的CD4（+）T细胞不能在刺激后调节CD40L表达可能占它们无法上调IgE水平的。为了在IL的存在下，作为K14-IL-4-TG / SKH1小鼠的CD19（+）B细胞分化为K14-IL-4-TG / SKH1小鼠的CD19（+）B细胞，与K14-IL-4-TG / CByB6小鼠合成相同量的IgE。 4和可溶性CD40L。我们的研究进一步表明，T细胞早期生长反应-1的缺陷可能对K14-IL-4-TG / SKH1小鼠中的CD40L上调受损。结论：K14-IL-4-TG / SKH1小鼠发育了类似人类内在特征性皮炎的皮肤炎症。因此，该模型可能适合于研究内在特征性皮炎的发病机制。

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