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首页> 外文期刊>Allergy >Role of cysteinyl leukotrienes in human allergen-specific Th2 responses induced by granulocyte macrophage-colony stimulating factor.
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Role of cysteinyl leukotrienes in human allergen-specific Th2 responses induced by granulocyte macrophage-colony stimulating factor.

机译：半胱氨酰白三烯在粒细胞巨噬细胞集落刺激因子诱导的人过敏原特异性Th2反应中的作用。

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BACKGROUND: The pro-inflammatory cytokine, granulocyte macrophage-colony stimulating factor (GM-CSF), which is elevated in the lungs of atopic asthmatic patients, has been shown to enhance major histocompatibility class II expression of alveolar macrophages (AM). We hypothesized that exposure of AM and monocytes from atopic asthmatic patients to GM-CSF would enhance their antigen presenting function, and investigated putative mechanisms for this effect. METHODS: Alveolar macrophages were purified from bronchoalveolar lavage by plastic adherence. Monocytes and CD4(+) T cells were purified from peripheral blood by magnetic bead separation. Antigen-presenting cell (APC) were pretreated with GM-CSF, pulsed with allergen and cocultured with autologous T cells. T-cell proliferation was determined by tritiated thymidine incorporation and cytokine production by enzyme-linked immunosorbent assay. RESULTS: Exposure of allergen-pulsed AM and peripheral blood monocytes to GM-CSF significantly increased allergen-specific T-cell proliferation and T helper 2 (Th2) cytokine production. The enhanced response was dependent on costimulation by CD86, but not CD80. Inhibition of the 5-lipoxygenase pathway abrogated GM-CSF-mediated upregulation by monocytes of allergen-specific interleukin-5 (IL-5) and IL-13 cytokine production. Blocking of the cysteinyl leukotriene receptor 1 (cysLT(1)) receptor by a specific receptor antagonist inhibited allergen-specific IL-5 production in response to GM-CSF pretreatment. CONCLUSION: Exposure to GM-CSF enhanced the capacity of human APC from atopic asthmatic patients to induce allergen-specific Th2 responses by a mechanism involving cysLT. Novel immunotherapies, targeting production of GM-CSF or its actions on APC have the potential, therefore, to prove beneficial in treatment of patients with inflammatory airway disease.
机译：背景：促炎性细胞因子粒细胞巨噬细胞集落刺激因子（GM-CSF）在特应性哮喘患者的肺中升高，已显示出可增强肺泡巨噬细胞（AM）的主要组织相容性II类表达。我们假设特应性哮喘患者将AM和单核细胞暴露于GM-CSF会增强其抗原呈递功能，并研究了这种作用的推测机制。方法：通过塑性粘附从支气管肺泡灌洗液中纯化肺泡巨噬细胞。通过磁珠分离从外周血中纯化单核细胞和CD4（+）T细胞。用GM-CSF预处理抗原呈递细胞（APC），用变应原脉冲处理，并与自体T细胞共培养。通过tri化的胸苷掺入和酶联免疫吸附法测定细胞因子的产生来确定T细胞的增殖。结果：过敏原脉冲的AM和外周血单核细胞暴露于GM-CSF显着增加了过敏原特异性T细胞增殖和T辅助2（Th2）细胞因子的产生。增强的响应取决于CD86的共刺激，而不取决于CD80。对5-脂氧合酶途径的抑制消除了变应原特异性白介素5（IL-5）和IL-13细胞因子产生的单核细胞对GM-CSF介导的上调。特定受体拮抗剂阻断半胱氨酰白三烯受体1（cysLT（1））受体抑制了响应GM-CSF预处理的变应原特异性IL-5的产生。结论：暴露于GM-CSF可通过涉及cysLT的机制增强特应性哮喘患者的人APC诱导过敏原特异性Th2反应的能力。因此，针对GM-CSF的产生或其对APC的作用的新型免疫疗法有潜力被证明对治疗炎症性气道疾病患者有益。

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