摘要
目的 研究树突状细胞 (DC)在抗曲霉菌免疫中的作用以及皮质类固醇如何在DC水平影响机体的抗曲霉菌免疫。方法 通过体外培养小鼠骨髓DC ,用麦氏比浊法检测DC对灭活曲霉菌孢子的吞噬量。酶联免疫吸附测定 (ELISA)检测DC以及脾脏T细胞分泌的细胞因子。结果 小鼠骨髓DC能高效吞噬加热灭活的曲霉菌孢子 ,皮质类固醇氢化可的松 (HC)抑制DC吞噬曲霉菌孢子的能力。DC受曲霉菌孢子刺激时分泌白细胞介素 12 (IL 12 )和干扰素γ(IFN γ) ,而不分泌白细胞介素 10 (IL 10 ) ,HC明显抑制DC分泌IL 12和IFN γ ,但不影响IL 10的分泌。给小鼠接种经灭活曲霉菌孢子冲击的DC后 ,其脾脏T细胞在体外受灭活曲霉菌孢子再刺激时分泌IFN γ ,而给小鼠接种经灭活曲霉菌孢子和HC联合冲击的DC后 ,其脾脏T细胞受灭活曲霉菌孢子再刺激时分泌IFN γ明显减少 ,IL 10却增加。结论 DC可能是抗曲霉菌免疫的效应细胞 ,并起始抗曲霉菌的Th1型免疫 ,HC抑制DC的这些功能 ,并使曲霉菌免疫偏向Th2型。经灭活曲霉菌孢子冲击的DC可能对增强免疫受损宿主抗曲霉菌免疫有作用。
Objective To investigate the role of dendritic cells(DCs) in host defense against aspergillus,and how corticosteroids hydrocortisone(HC) affects host anti-aspergillus immunity at the DCs level. Methods Mouse bone marrow-derived DCs were generated ex vivo and the uptake of inactivated Aspergillus fumigatus conidia (iAfc) by DCs was assayed using McFar-Land standard. Cytokine production by DCs or by splenic T cells were measured using ELISA method. Results DCs were capable of ingesting iAfc efficiently. HC significantly inhibited the capacity of DCs to phagocytose iAfc. After stimulated with iAfc in vitro,DCs secreted IL-12 and IFN-γ,but did not secret IL-10. 10 -5 mol/L HC down-regulated IL-12 and IFN-γ production by DCs,but it didn′t affect IL-10 production. After the mice were inoculated with iAfc-pulsed DCs,their splenic T cells secreted IFN-γ upon the re-stimulation with iAfc in vitro. In contrast,after the mice were inoculated with iAfc-HC-pulsed DCs,the splenic T cells showed significantly decreased IFN-γ secretion upon the same stimulation,but the secretion of IL-10 was increased. Conclusions DCs might act as effector cells in host defense against aspergillus,and initiate anti-aspergillus Th1 type immunity. HC inhibited the above functions of DCs and skew the immunity response towords Th2 type. iAfc-pulsed DCs migth be useful for promoting the anti-aspergillus immunity of immunocompromised host.
出处
《中华结核和呼吸杂志》
CAS
CSCD
北大核心
2004年第7期449-454,共6页
Chinese Journal of Tuberculosis and Respiratory Diseases
基金
上海市卫生系统百人计划基金资助项目 (RB0 3 0 )
