Altare F, Durandy A, Lammas D, Emile J F, Lamhamedi S, Le Deist F, Drysdale P, Jouanguy E, Döffinger R, Bernaudin F, Jeppsson O, Gollob J A, Meinl E, Segal A W, Fischer A, Kumararatne D, Casanova J L
INSERM U429, Hôpital Necker-Enfants Malades, Paris 75015, France.
Science. 1998 May 29;280(5368):1432-5. doi: 10.1126/science.280.5368.1432.
In humans, interferon gamma (IFN-gamma) receptor deficiency leads to a predisposition to mycobacterial infections and impairs the formation of mature granulomas. Interleukin-12 (IL-12) receptor deficiency was found in otherwise healthy individuals with mycobacterial infections. Mature granulomas were seen, surrounded by T cells and centered with epithelioid and multinucleated giant cells, yet reduced IFN-gamma concentrations were found to be secreted by activated natural killer and T cells. Thus, IL-12-dependent IFN-gamma secretion in humans seems essential in the control of mycobacterial infections, despite the formation of mature granulomas due to IL-12-independent IFN-gamma secretion.
在人类中,γ干扰素(IFN-γ)受体缺陷会导致易患分枝杆菌感染,并损害成熟肉芽肿的形成。在患有分枝杆菌感染的其他方面健康的个体中发现了白细胞介素-12(IL-12)受体缺陷。可见成熟的肉芽肿,周围有T细胞,中心为上皮样细胞和多核巨细胞,但发现活化的自然杀伤细胞和T细胞分泌的IFN-γ浓度降低。因此,尽管存在不依赖IL-12的IFN-γ分泌导致成熟肉芽肿的形成,但人类中依赖IL-12的IFN-γ分泌似乎对控制分枝杆菌感染至关重要。