Palma Carla, Spallek Ralf, Piccaro Giovanni, Pardini Manuela, Jonas Fatima, Oehlmann Wulf, Singh Mahavir, Cassone Antonio
Department of Infectious, Parasitic and Immune-Mediated Diseases, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy.
Clin Dev Immunol. 2011;2011:690328. doi: 10.1155/2011/690328. Epub 2011 Mar 27.
The M. tuberculosis phosphate-binding transporter lipoproteins PstS1 and PstS3 were good immunogens inducing CD8(+) T-cell activation and both Th1 and Th17 immunity in mice. However, this antigen-specific immunity, even when amplified by administration of the protein with the adjuvant LTK63 or by the DNA priming/protein boosting regimen, was not able to contain M. tuberculosis replication in the lungs of infected mice. The lack of protection might be ascribed with the scarce/absent capacity of PstS1/PstS3 antigens to modulate the IFN-γ response elicited by M. tuberculosis infection during which, however, PstS1-specific IL-17 secreting cells were generated in both unvaccinated and BCG-vaccinated mice. In spite of a lack of protection by PstS1/PstS3 immunizations, our results do show that PstS1 is able to induce IL-17 response upon M. tuberculosis infection which is of interest in the study of anti-M. tuberculosis immunity and as potential immunomodulator in combined vaccines.
结核分枝杆菌的磷酸结合转运脂蛋白PstS1和PstS3是良好的免疫原，可诱导小鼠CD8(+) T细胞活化以及Th1和Th17免疫。然而，这种抗原特异性免疫，即使通过与佐剂LTK63一起给予蛋白质或通过DNA初免/蛋白质加强方案进行增强，也无法抑制感染小鼠肺部的结核分枝杆菌复制。缺乏保护作用可能归因于PstS1/PstS3抗原调节结核分枝杆菌感染引发的IFN-γ反应的能力不足/缺乏，不过，在未接种疫苗和接种卡介苗的小鼠中均产生了分泌PstS1特异性IL-17的细胞。尽管PstS1/PstS3免疫缺乏保护作用，但我们的结果确实表明，PstS1能够在结核分枝杆菌感染后诱导IL-17反应，这在抗结核分枝杆菌免疫研究以及联合疫苗中作为潜在免疫调节剂方面具有重要意义。
