Kossodo S, Monso C, Juillard P, Velu T, Goldman M, Grau G E
Department of Anaesthesiology, University of Geneva, Switzerland.
Immunology. 1997 Aug;91(4):536-40. doi: 10.1046/j.1365-2567.1997.00290.x.
In this study, we examined the effects of interleukin-10 (IL-10) on the outcome of experimental cerebral malaria (CM), a lethal neurological syndrome that occurs in susceptible strains of mice after infection with Plasmodium berghei ANKA (PbA). Constitutive IL-10 mRNA levels were significantly higher in the spleen and brain of resistant animals. In vivo neutralization of endogenous IL-10 in CM-resistant mice induced the neurological syndrome in 35.7% of these mice, as opposed to 7.7% in controls. IL-10 inhibited PbA antigen-specific interferon-gamma (IFN-gamma) production in vitro but not tumour necrosis factor (TNF) serum levels in vivo. Susceptible mice, on the other hand, were significantly protected against CM when injected with recombinant IL-10. Overall, our findings suggest that IL-10 plays a protective role against experimental cerebral malaria.
在本研究中，我们检测了白细胞介素-10（IL-10）对实验性脑型疟疾（CM）结局的影响，CM是一种致命的神经综合征，在感染伯氏疟原虫ANKA（PbA）后，易感品系小鼠中会出现该综合征。抗性动物脾脏和大脑中组成型IL-10 mRNA水平显著更高。在CM抗性小鼠体内对内源性IL-10进行中和，导致35.7%的此类小鼠出现神经综合征，而对照组为7.7%。IL-10在体外抑制PbA抗原特异性干扰素-γ（IFN-γ）的产生，但在体内不影响肿瘤坏死因子（TNF）血清水平。另一方面，易感小鼠注射重组IL-10后，可显著预防CM。总体而言，我们的研究结果表明，IL-10对实验性脑型疟疾起保护作用。
