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首页> 外文期刊>American journal of rhinology >Signals through CD40 play a critical role in the pathophysiology of Schistosoma mansoni egg antigen--induced allergic rhinitis in mice.
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Signals through CD40 play a critical role in the pathophysiology of Schistosoma mansoni egg antigen--induced allergic rhinitis in mice.

机译：通过CD40发出的信号在曼氏血吸虫卵抗原诱发的小鼠过敏性鼻炎的病理生理中起着至关重要的作用。

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BACKGROUND: Interaction between CD40 and CD40L is thought to regulate immune responses in several allergic diseases. However, little is known about its in vivo role in the pathophysiology of allergic rhinitis. We sought to determine whether the lack of signals through CD40 affects the pathophysiology of allergic rhinitis using a murine model. METHODS: Wild type (WT) and CD40-deficient BALB/c (CD40-/-) mice were sensitized intranasally to Schistosoma mansoni egg antigen (SEA). After repeated sensitization, histamine responsiveness, serum antibody titer including immunoglobulin E (IgE), nasal eosinophilia, and cytokine production by nasal mononuclear cells were determined in each group. RESULTS: Intranasal sensitization with SEA in WT mice elicited a strong Th2 response including SEA-specific IgE production, nasal eosinophilia, and interleukin (IL)-4, and IL-5 production by nasal mononuclear cells after antigen challenge. Production of SEA-specific IgE and IgG1 was abolished in SEA-sensitized CD40-/- mice. These mice showed impaired nasal eosinophilia and displayed markedly reduced histamine-induced nasal hyperresponsiveness as compared with WT mice. Furthermore, reduced production of IL-4 and IL-5 by nasal mononuclear cells was seen in CD40-/- mice. CONCLUSION: These results show that signals through CD40 play a critical role in not only IgE production but also pathophysiology of allergic rhinitis such as nasal hyperresponsiveness and nasal eosinophilia.
机译：背景：CD40和CD40L之间的相互作用被认为可以调节几种过敏性疾病的免疫反应。然而，关于其在变应性鼻炎的病理生理中的体内作用了解甚少。我们试图通过鼠模型来确定缺乏通过CD40的信号是否影响变应性鼻炎的病理生理。方法：将野生型（WT）和CD40缺陷型BALB / c（CD40-/-）小鼠经鼻内敏化曼氏血吸虫卵抗原（SEA）。反复敏化后，确定每组中的组胺反应性，包括免疫球蛋白E（IgE）的血清抗体滴度，鼻嗜酸性粒细胞增多和鼻单核细胞产生的细胞因子。结果：野生型小鼠的SEA鼻内敏化引起强烈的Th2应答，包括SEA特异性IgE产生，鼻嗜酸性粒细胞增多和白介素（IL）-4以及抗原攻击后鼻单核细胞产生IL-5。 SEA敏感的CD40-/-小鼠取消了SEA特异性IgE和IgG1的产生。与野生型小鼠相比，这些小鼠的鼻嗜酸性粒细胞减少，并且组胺诱导的鼻高反应性明显降低。此外，在CD40-/-小鼠中观察到鼻单核细胞产生的IL-4和IL-5减少。结论：这些结果表明，通过CD40发出的信号不仅在IgE产生中起着关键作用，而且在变应性鼻炎的病理生理学（例如鼻高反应性和鼻嗜酸性粒细胞增多）中也起着至关重要的作用。

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