Openshaw P J, Hussell T
Imperial College, St Mary's Hospital, London, U.K.
Dev Biol Stand. 1998;92:179-85.
In humans and mice, sensitisation to respiratory syncytial virus (RSV) antigens can result in severe inflammatory lung disease during subsequent infection with the virus. Although specific antiviral T cells are thought to be responsible for this augmentation of disease, the precise role of different functional subsets is unknown. BALB/c mice sensitised to the major surface glycoprotein (G) of RSV expressed by recombinant vaccinia virus develop Th2-driven lung eosinophilia after intranasal challenge with the virus. Mice treated with IL-12 at various times during vaccination and challenge, had reduced vaccine-induced lung eosinophilia but increased total pulmonary lymphoid cell infiltration. Intracellular cytokine analysis showed that interferon-gamma production during challenge was increased and IL-4 and IL-5 reduced by IL-12 treatment. Though IL-12 treatment reduced lung eosinophilia, illness (as assessed by weight loss) was not eliminated and sometimes increased. Reversing Th2-associated pathology with IL-12 does not necessarily benefit the host.
在人类和小鼠中，对呼吸道合胞病毒（RSV）抗原致敏可导致在随后感染该病毒期间出现严重的炎症性肺病。尽管特定的抗病毒T细胞被认为是这种疾病加重的原因，但不同功能亚群的确切作用尚不清楚。用重组痘苗病毒表达的RSV主要表面糖蛋白（G）致敏的BALB/c小鼠，在经鼻用该病毒攻击后会出现Th2驱动的肺部嗜酸性粒细胞增多。在接种疫苗和攻击期间的不同时间用IL-12治疗的小鼠，疫苗诱导的肺部嗜酸性粒细胞增多减少，但肺内总淋巴细胞浸润增加。细胞内细胞因子分析表明，攻击期间干扰素-γ的产生增加，而IL-12治疗使IL-4和IL-5减少。虽然IL-12治疗减少了肺部嗜酸性粒细胞增多，但疾病（通过体重减轻评估）并未消除，有时反而加重。用IL-12逆转与Th2相关的病理变化不一定对宿主有益。
