目的观察小鼠皮肤着色真菌病模型发病过程中TNF-α和IFN-γ基因表达的动态变化,并进一步探讨其在宿主防御机制中的作用。方法 ICR小鼠分为4组,A组为健康小鼠足垫皮下接种卡氏支孢霉悬液组;B组为免疫抑制小鼠足垫皮下接种卡氏支孢霉悬液组;C组为免疫抑制小鼠足垫皮下接种灭活卡氏支孢霉悬液组;D组为健康小鼠足垫皮下接种生理盐水做对照。接种后第7、30、60d时RT-PCR法检测小鼠皮损组织TNF-α、IFN-γ的mRNA表达水平。结果 A组TNF-α基因表达水平在接种后第7、30、60d分别为2.552±0.5342、1.6740±0.4106、1.4900±0.5612,第30d较第7d显著下降(P<0.05),但较第60d无显著差异(P>0.05)。B组在接种后第7、30d分别为1.8120±0.3725、1.4620±0.3142,两者无显著差异(P>0.05),第60d为1.5420±0.4280,与第30d无显著差异(P>0.05)。C组在接种后第7、30d分别为1.8800±0.3697、1.3100±0.4594,两者无显著差异(P>0.05),第60d为1.4000±0.3595,与第30d无显著差异(P>0.05)。A组IFN-γ基因表达水平在接种后第7、30d分别为0.5160±0.1126、0.9680±0.1946,后者较前者显著上升(P<0.005),第60d为1.2100±0.2107,较第30d无显著差异(P>0.05)。B组在接种后第7d、30d分别为0.2920±0.1482、0.7640±0.1823,后者较前者显著上升(P<0.005),第60d为1.0920±0.5102,较第30d无显著差异(P>0.05)。C组在接种后第7、30d分别为0.2780±0.1937、0.8900±0.3580,后者较前者显著上升(P<0.05),第60d为1.100±0.3808,与30d相比无显著性差异(P>0.05)。D组TNF-α和IFN-γ则无显著改变(P>0.05)。结论在卡氏支孢霉所致的着色真菌病模型的发病过程中有TNF-α和IFN-γ的参与。感染早期TNF-α、IFN-γ可能协同加强Th1型反应清除感染部位的真菌,从而起对机体保护作用。 Objective To observe the dynamic changes of TNF-α and IFN-γ gene expression during the development of skin pigmented mycosis model in mice and to explore its role in the host defense mechanism. Methods ICR mice were divided into 4 groups: group A was subcutaneously inoculated with C. carinii suspension in foot pad of healthy mice; group B was subcutaneously inoculated with C. cardiomyces suspension group in foot pad of immunosuppressive mice; group C The immunosuppressive mice were inoculated subcutaneously inoculated with Mycosphaerella & instillation suspension to the foot pad. The healthy mice were subcutaneously inoculated with normal saline as control. At the 7th, 30th, 60th and 60th day after inoculation, the mRNA expressions of TNF-α and IFN-γ in the skin lesions were detected by RT-PCR. Results The level of TNF-α gene expression in group A was 2.552 ± 0.5342, 1.6740 ± 0.4106 and 1.4900 ± 0.5612 respectively at the 7th, 30th and 60th day after inoculation, and significantly decreased at the 30th day compared with the 7th day (P <0.05) Significant difference (P> 0.05). There was no significant difference between the two groups at the 7th and 30th day after inoculation (P> 0.05), and at the 60th day was 1.5420 ± 0.4280 (P> 0.05). There was no significant difference between the two groups at the 7th and 30th day after inoculation (P> 0.05). The 60th day was 1.4000 ± 0.3595, which was not significantly different from the 30th day (P> 0.05). The expression of IFN-γ in group A was 0.5160 ± 0.1126,0.9680 ± 0.1946 on the 7th and 30th day after inoculation, the latter was significantly higher than the former (P <0.005), and on the 60th day was 1.2100 ± 0.2107, which was not significantly different from the 30th day (P> 0.05). On the 7th day and the 30th day after inoculation, the B group was 0.2920 ± 0.1482 and 0.7640 ± 0.1823, respectively. The latter group was significantly higher than the former (P <0.005), and the 60th day was 1.0920 ± 0.5102, which was not significantly different from the 30th day (P> 0.05). The C group was 0.2780 ± 0.1937,0.8900 ± 0.3580 on the 7th and 30th day after inoculation, the latter was significantly higher than the former (P <0.05), and the 60th day was 1.100 ± 0.3808, no significant difference compared with the 30th day (P> 0.05 ). There was no significant change in TNF-α and IFN-γ in group D (P> 0.05). Conclusion TNF-α and IFN-γ are involved in the pathogenesis of mycosis fungoides caused by Mycobacterium card. Early infection of TNF-α, IFN-γ may synergistically enhance the Th1-type response to clear the infected parts of the fungus, which play a protective role on the body.