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目的研究C5a/C5aR通路在对硕大利什曼原虫(Leishmania major,L.major)易感的BALB/c小鼠免疫病理发生中的作用及机制探讨。方法以C5aR KO小鼠(BALB/c背景)为模型,观察比较了WT和C5aR KO的BALB/c小鼠在L.major感染后的病变情况,有限稀释法检测了各组感染小鼠体内寄生虫的负荷,并进一步通过FACS检测了相关细胞因子如IL-17和IL-4的产生,来探讨C5a/C5aR通路在L.major易感型BALB/c小鼠免疫病理发生中的作用机制。结果相比WT小鼠,C5aRKO小鼠感染L.major后的病变程度明显减轻(P<0.05),体内寄生虫负荷也显著降低(6.952±0.398vs 4.340±0.434,P<0.01);同时,FACS胞内染色结果表明CD4+IL-4+T细胞亚群百分比显著降低(0.960 0±0.148 3 vs0.314 0±0.042 6,P<0.01),但CD3+IL-17+T细胞亚群的百分比在两组之间无显著差异(0.792 0±0.051 3 vs 0.858 0±0.084 5,P=0.522 3)。结论 C5a/C5aR通路通过调节Th2细胞关键细胞因子IL-4的产生,在L.major易感小鼠的免疫病理发生中发挥作用。
Objective To investigate the role and mechanism of C5a / C5aR pathway in the immunopathogenesis of BALB / c mice susceptible to Leishmania major (L. major). Methods C5aR KO mice (BALB / c background) were used as a model to observe the pathological changes of BALB / c mice infected with WT and C5aR KO after L. major infection. The limited dilution method was used to detect the parasites To investigate the mechanism of C5a / C5aR pathway in the immunopathogenesis of L. major-susceptible BALB / c mice by FACS analysis of the production of related cytokines such as IL-17 and IL-4. Results Compared with WT mice, C5aRKO mice showed a significant reduction of pathological changes (P <0.05) and a significant decrease in parasitic burden (6.952 ± 0.398 vs 4.340 ± 0.434, P <0.01). In contrast, FACS Intracellular staining showed that the percentage of CD4 + IL-4 + T cell subsets was significantly decreased (0.960 ± 0.148 3 vs. 0.34 ± 0.042 6, P <0.01), but the percentage of CD3 + IL-17 + T cell subsets There was no significant difference between the two groups (0.792 ± 0.051 3 vs 0.858 ± 0.084 5, P = 0.522 3). Conclusion The C5a / C5aR pathway plays a role in the immunopathogenesis of L. major susceptible mice by regulating the production of IL-4, a key cytokine of Th2 cells.