Jouanguy E, Döffinger R, Dupuis S, Pallier A, Altare F, Casanova J L
Institut National de la Santé et de la Recherche Médicale Unité 429,Hôpital Necker-Enfants Malades, 149 rue de Sèvres, 75015, Paris, France, EU.
Curr Opin Immunol. 1999 Jun;11(3):346-51. doi: 10.1016/s0952-7915(99)80055-7.
The development of gene-knockout mice and the identification of gene-deficient humans have improved our understanding of the role of IL-12 and IFN-gamma in host defense. Comparison of experimental and natural infections has shown that animals and humans genetically deficient in immunity mediated by IL-12 or IFN-gamma are highly susceptible to mycobacteria and salmonella. Impaired secretion of, or response to, IFN-gamma is the common pathogenic mechanism that accounts for impaired granuloma formation and uncontrolled growth of bacteria within macrophages. The axis formed between IL-12 and IFN-gamma is essential for protective immunity against mycobacteria and salmonella in mice and men.
基因敲除小鼠的培育以及基因缺陷人类的鉴定，增进了我们对白细胞介素-12（IL-12）和γ干扰素（IFN-γ）在宿主防御中作用的理解。对实验性感染和自然感染的比较表明，在由IL-12或IFN-γ介导的免疫方面存在基因缺陷的动物和人类，对分枝杆菌和沙门氏菌高度易感。IFN-γ分泌受损或对其反应受损，是导致肉芽肿形成受损以及巨噬细胞内细菌生长失控的常见致病机制。IL-12和IFN-γ之间形成的轴，对于小鼠和人类抵抗分枝杆菌和沙门氏菌的保护性免疫至关重要。
