MacLennan Calman, Fieschi Claire, Lammas David A, Picard Capucine, Dorman Susan E, Sanal Ozden, MacLennan Jenny M, Holland Steven M, Ottenhoff Tom H M, Casanova Jean-Laurent, Kumararatne Dinakantha S
Medical Research Council Centre for Immune Regulation, Division of Immunity and Infection, University of Birmingham, Birmingham, Alabama, USA.
J Infect Dis. 2004 Nov 15;190(10):1755-7. doi: 10.1086/425021. Epub 2004 Oct 7.
Patients with inherited deficiency of the interleukin (IL)-12/IL-23-interferon (IFN)- gamma axis show increased susceptibility to invasive disease caused by the intramacrophage pathogens salmonellae and mycobacteria. We analyzed data on 154 patients with such deficiency. Significantly more patients with IL-12/IL-23-component deficiency had a history of salmonella disease than did those with IFN- gamma -component deficiency. Salmonella disease was typically severe, extraintestinal, and caused by nontyphoidal serovars. These findings strongly suggest that IL-12/IL-23 is a key cytokine for immunity against salmonella in humans and that IL-12/IL-23 mediates this protective effect partly through IFN- gamma -independent pathways. Investigation of the IL-12/IL-23-IFN- gamma axis should be considered in patients with invasive salmonella disease.
白细胞介素（IL）-12/IL-23-干扰素（IFN）-γ轴存在遗传性缺陷的患者，对巨噬细胞内病原体沙门氏菌和分枝杆菌引起的侵袭性疾病易感性增加。我们分析了154例有此类缺陷患者的数据。与IFN-γ成分缺陷患者相比，IL-12/IL-23成分缺陷患者有沙门氏菌病病史的显著更多。沙门氏菌病通常病情严重、为肠外感染且由非伤寒血清型引起。这些发现有力地表明，IL-12/IL-23是人类抗沙门氏菌免疫的关键细胞因子，且IL-12/IL-23部分通过不依赖IFN-γ的途径介导这种保护作用。对于侵袭性沙门氏菌病患者，应考虑对IL-12/IL-23-IFN-γ轴进行检查。
