Rook Graham A W, Hernandez-Pando Rogelio, Dheda Keertan, Teng Seah Geok
Centre for Infectious Diseases and International Health, Windeyer Institute for Medical Sciences, Royal Free and University College Medical School, 46 Cleveland Street, London, UK.
Trends Immunol. 2004 Sep;25(9):483-8. doi: 10.1016/j.it.2004.06.005.
Current attempts to find a vaccine for tuberculosis (TB) are based on the assumption that it must drive a Th1 response. We review the evidence that progressive disease might not be due to absence of Th1, but rather to the subversive effect of an unusual Th2-like response, involving interleukin-4 (IL-4) and IL-4delta2. This Th2-like response can impair bactericidal function and lead to toxicity of tumour necrosis factor-alpha (TNF-alpha) and to pulmonary fibrosis. If this is important, effective vaccines will need to suppress pre-existing Th2-like activity. Such vaccines are feasible and are active therapeutically in mouse TB.
目前寻找结核病疫苗的尝试基于这样一种假设,即该疫苗必须激发Th1反应。我们回顾了相关证据,即疾病进展可能并非由于缺乏Th1,而是由于一种不寻常的类似Th2反应的破坏作用,这种反应涉及白细胞介素-4(IL-4)和IL-4δ2。这种类似Th2的反应会损害杀菌功能,并导致肿瘤坏死因子-α(TNF-α)毒性和肺纤维化。如果这一点很重要,那么有效的疫苗将需要抑制已有的类似Th2的活性。此类疫苗是可行的,并且在小鼠结核病中具有治疗活性。