Department of Immunology, Yokohama City University School of Medicine, Kanagawa, Japan.
Allergol Int. 2009 Sep;58(3):445-54. doi: 10.2332/allergolint.08-OA-0081. Epub 2009 Jul 25.
Influenza A viral infection is concerned with induction of asthma. CD11c+ pulmonary antigen presenting cells (APCs) play a central role in sensitization with inhaled antigens during the acute phase of influenza A viral infection and also reside on bronchial epithelium for the long term after sensitization. To investigate the role of CD11c+ pulmonary APCs in the inhaled antigen sensitization during the acute phase of influenza A viral infection, we analyzed their function.
Mice were infected with influenza A virus and were sensitized intranasally with BSA/alum during the acute phase of influenza A viral infection. Expression of surface antigens on CD11c+ pulmonary APCs was analyzed by FACS. Cytokine production from CD11c+ pulmonary APCs, and interaction between CD11c+ pulmonary APCs and naïve CD4+ T cells was assessed by ELISA. Ability of antigen presentation by CD11c+ pulmonary APCs was measured by proliferation assay.
BSA antigen sensitization during the acute phase of influenza A viral infection induced eosinophil recruitment into the lungs after BSA antigen challenge and moderately increased expression of MHC class II molecules on CD11c+ pulmonary APCs. The interaction between the CD11c+ pulmonary APCs and naïve CD4+ T cells secreted large amounts of IL-10.
BSA antigen sensitization during the acute phase of influenza A viral infection enhanced IL-10 production from naïve CD4+ T cell interaction with CD11c+ pulmonary APCs. The IL-10 secretion evoked Th2 responses in the lungs with downregulation of Th1 responses and was important for the eosinophil recruitment into the lungs after BSA antigen challenge.
甲型流感病毒感染与哮喘的诱导有关。CD11c+肺抗原呈递细胞（APCs）在甲型流感病毒感染的急性期吸入抗原致敏过程中发挥核心作用，并且在致敏后长期存在于支气管上皮细胞上。为了研究 CD11c+肺 APCs 在甲型流感病毒感染急性期吸入抗原致敏中的作用，我们分析了它们的功能。
小鼠感染甲型流感病毒，并在甲型流感病毒感染的急性期经鼻腔内用 BSA/明矾进行致敏。通过 FACS 分析 CD11c+肺 APCs 表面抗原的表达。通过 ELISA 评估 CD11c+肺 APCs 的细胞因子产生以及 CD11c+肺 APCs 与幼稚 CD4+T 细胞之间的相互作用。通过增殖测定评估 CD11c+肺 APCs 的抗原呈递能力。
BSA 抗原在甲型流感病毒感染的急性期致敏可在 BSA 抗原攻击后诱导嗜酸性粒细胞募集到肺部，并适度增加 CD11c+肺 APCs 上 MHC Ⅱ类分子的表达。CD11c+肺 APCs 与幼稚 CD4+T 细胞之间的相互作用会分泌大量的 IL-10。
BSA 抗原在甲型流感病毒感染的急性期致敏增强了幼稚 CD4+T 细胞与 CD11c+肺 APCs 相互作用时产生的 IL-10。这种 IL-10 分泌在肺部引发了 Th2 反应，下调了 Th1 反应，是 BSA 抗原攻击后嗜酸性粒细胞募集到肺部的重要因素。
