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Participation of CD11b and F4/80 molecules in the conjunctival eosinophilia of experimental allergic conjunctivitis.

机译:CD11b和F4 / 80分子参与实验性变应性结膜炎的结膜嗜酸性粒细胞增多症。

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BACKGROUND: CD11b and F4/80 are macrophage surface markers. How these molecules participate in allergic eosinophil infiltration remains unclear. We examined the roles CD11b and F4/80 play in the conjunctival eosinophil infiltration associated with experimental allergic conjunctivitis. METHODS: Ragweed-immunized BALB/c mice were challenged with ragweed in eye drops to induce conjunctival eosinophil infiltration. The effect of challenge on conjunctival CD11b+ and F4/80+ cell numbers was determined by immunohistochemistry. In the same model, blocking anti-CD11b and anti-F4/80 Abs were injected intraperitoneally during the induction or the effector phase, or subconjunctivally 2 h before challenge, to determine their effect on challenge-induced conjunctival eosinophilia. To examine whether eosinophils express CD11b and F4/80 molecules, splenocytes from IL-5 gene-electroporated mice were subjected to flow cytometric analysis. To clarify the involvement of CD11b and F4/80 in conjunctival eosinophil infiltration, mice were intraperitoneally injected with anti-CD11b and anti-F4/80 Abs and then subconjunctivally injected with eotaxin to induce conjunctival eosinophilia. RESULTS: Ragweed challenge elevated conjunctival CD11b+ and F4/80+ cell numbers. Systemic anti-CD11b and anti-F4/80 Ab treatments during the effector phase, but not in either the induction phase or the local injection of Ab, suppressed conjunctival eosinophil infiltration in ragweed-induced conjunctivitis. Most splenic eosinophils from IL-5 gene-introduced mice expressed CD11b and F4/80. Systemic anti-CD11b and anti-F4/80 Ab treatment suppressed conjunctival eosinophilia induced by subconjunctival eotaxin injection. CONCLUSIONS: CD11b and F4/80 appear to participate in conjunctival eosinophil infiltration in allergic conjunctivitis. Their involvement in conjunctival eosinophilia appears to be due to their expression on eosinophils rather than on macrophages.
机译:背景:CD11b和F4 / 80是巨噬细胞表面标志物。这些分子如何参与过敏性嗜酸性粒细胞浸润尚不清楚。我们检查了CD11b和F4 / 80在与实验性变应性结膜炎相关的结膜嗜酸性粒细胞浸润中的作用。方法:用豚草滴眼液攻击豚草免疫的BALB / c小鼠,以诱导结膜嗜酸性粒细胞浸润。通过免疫组织化学确定攻击对结膜CD11b +和F4 / 80 +细胞数量的影响。在同一模型中,在诱导或效应期或攻击前结膜下结膜下腹膜内注射阻断性抗CD11b和抗F4 / 80 Abs,以确定它们对攻击诱导的结膜嗜酸性粒细胞的影响。为了检查嗜酸性粒细胞是否表达CD11b和F4 / 80分子,对来自IL-5基因电穿孔小鼠的脾细胞进行了流式细胞仪分析。为了阐明CD11b和F4 / 80参与结膜嗜酸性粒细胞浸润,小鼠腹膜内注射了抗CD11b和抗F4 / 80 Abs,然后结膜下注射了嗜酸性粒细胞趋化因子诱导结膜嗜酸性粒细胞增多。结果:豚草攻击结膜CD11b +和F4 / 80 +细胞数量增加。在效应期,而不是在诱导期或局部注射Ab时,全身性抗CD11b和抗F4 / 80 Ab治疗抑制豚草诱导的结膜炎中结膜嗜酸性粒细胞浸润。来自IL-5基因导入小鼠的大多数脾嗜酸性粒细胞表达CD11b和F4 / 80。全身抗CD11b和抗F4 / 80 Ab治疗抑制了结膜下嗜酸性粒细胞趋化因子注射引起的结膜嗜酸性粒细胞增多。结论:CD11b和F4 / 80似乎参与了过敏性结膜炎的结膜嗜酸性粒细胞浸润。它们参与结膜性嗜酸性粒细胞增多似乎是由于它们在嗜酸性粒细胞而不是巨噬细胞上表达。

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