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目的:探讨阻断CD40-CD40配体共刺激信号诱导移植免疫耐受对树突状细胞功能的影响。方法:将抗CD40配体抗体(MR-1)应用于小鼠心脏移植受体以诱导移植免疫耐受,使用磁珠细胞提取装置从排斥及免疫耐受受体中提取树突状细胞。使用流式细胞仪测定树突状细胞表面分子CD40、CD80及CD86的表达。于体外以LPS再刺激树突状细胞,并使用ELISA法测定上清中的细胞因子IL-10和IL-12的水平。同时采用混合淋巴细胞反应(MLR)测定了树突状细胞的刺激性及免疫调节能力。结果:免疫耐受受体的树突状细胞表达低水平的共刺激分子CD40、CD80及CD86,同时分泌高水平的IL-10和低水平的IL-12。而且这些树突状细胞具有较弱的刺激性,并能抑制脾细胞的增殖。结论:阻断CD40-CD40配体共刺激信号可以产生免疫耐受状态,在这样的免疫耐受受体中诱导出未成熟表型的IL-10highIL-12low树突状细胞,这些细胞具有免疫调节活性。
OBJECTIVE: To investigate the effect of blockade of CD40-CD40 ligand co-stimulatory signal on the function of dendritic cells induced by transplantation immune tolerance. Methods: Anti-CD40 ligand antibody (MR-1) was applied to mouse heart transplant recipients to induce transplantation tolerance. Dendritic cells were extracted from rejection and immune tolerant recipients using magnetic bead cell extraction equipment. Flow cytometry was used to determine the expression of dendritic cell surface molecules CD40, CD80 and CD86. Dendritic cells were restimulated with LPS in vitro and the levels of cytokines IL-10 and IL-12 in the supernatant were measured by ELISA. Simultaneous mixed lymphocyte reaction (MLR) was used to determine the stimulatory and immunomodulatory capacity of dendritic cells. RESULTS: Immune tolerant recipients dendritic cells expressed low levels of costimulatory molecules CD40, CD80 and CD86, secreting high levels of IL-10 and low levels of IL-12. Moreover, these dendritic cells have weaker irritation and can inhibit the proliferation of spleen cells. Conclusion: Blocking the CD40-CD40 ligand co-stimulatory signal can produce immune tolerance states in which immature phenotypes of IL-10 highIL-12low dendritic cells are induced that have immunomodulatory active.