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目的 探讨干扰素 γ(IFN γ)对小鼠抗日本血吸虫感染保护力的机制。 方法 采用高密度寡核苷酸芯片 (Affymetrix芯片 )结合半定量逆转录 聚合酶链反应 (RT PCR )方法 ,对BALB/c小鼠感染日本血吸虫过程中脾脏CD4+ T细胞进行基因转录水平分析 ,获得IFN γ诱导鸟苷三磷酸 (GTP)酶家族成员的变化图谱 ;并对其中IFN γ诱导GTP酶 (IGTP)进行分子克隆和序列测定。 结果 小鼠自然感染日本血吸虫过程中 ,IFN γ诱导GTP酶家族成员的基因表达呈现特征性变化 ,感染后 3wk ,基因表达上调或变化不显著 ;感染后 6wk至 13wk ,基因表达持续受到抑制。这种变化特征经RT PCR方法所证实。从小鼠脾脏可扩增出IGTP全长基因 ,但退火温度降低时出现IGTP基因转录缺失。 结论 小鼠急性感染日本血吸虫后 ,体内IFN γ通路逐步受到抑制 ,针对血吸虫感染的依赖IFN γ的抗感染保护力下降
Objective To investigate the mechanism of interferon γ (IFN γ) in protecting mice against infection by Schistosoma japonicum. Methods The gene transcription level of splenic CD4 + T cells from BALB / c mice infected with Schistosoma japonicum was analyzed by high-density oligonucleotide microarray (Affymetrix chip) combined with semi-quantitative reverse transcriptase-polymerase chain reaction (RT PCR) IFNγ induced changes in the guanosine triphosphate (GTP) enzyme family members; and IFNγ-induced GTPase (IGTP) molecular cloning and sequencing. Results In the natural infection of Schistosoma japonicum, IFNγ induced the expression of GTPase family members. The gene expression was not significantly changed at 3 weeks after infection. The expression of GTPase gene was inhibited continuously from 6wk to 13wk after infection. This variation was confirmed by RT PCR. IGTP full-length gene can be amplified from mouse spleen, but IGTP gene transcription loss occurs when the annealing temperature is decreased. Conclusions The in vivo IFNγ pathway is gradually inhibited in mice after acute infection with Schistosoma japonicum, and the protective ability against IFNγ-dependent infection against schistosoma infection is decreased