Development of spontaneous airway changes consistent with human asthma in mice lacking T-bet
Development of spontaneous airway changes consistent with human asthma in mice lacking T-bet
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DOI：
10.1126/science.1065544
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发表时间：
2002-01-11
期刊：
影响因子：
56.9
通讯作者：
Glimcher, LH
中科院分区：
文献类型：
--
作者：
Finotto, S;Neurath, MF;Glimcher, LH
人类哮喘与辅助性T(H)2淋巴细胞的气道浸润有关。我们观察到来自哮喘患者气道的T细胞中T(H)1转录因子T-bet的表达低于来自非哮喘患者气道的T细胞，这表明T-bet的缺失可能与哮喘有关。靶向缺失T-bet基因的小鼠和接受T-bet敲除小鼠CD4（+）细胞的严重联合免疫缺陷小鼠自发地表现出哮喘的多种生理和炎症特征，因此，在没有过敏原暴露的情况下，T-bet缺陷诱导小鼠表型与急性和慢性人类哮喘相似。
Human asthma is associated with airway infiltration by T helper 2 (T(H)2) lymphocytes. We observed reduced expression of the T(H)1 transcription factor, T-bet, in T cells from airways of patients with asthma compared with that in T cells from airways of nonasthmatic patients, suggesting that loss of T-bet might be associated with asthma. Mice with a targeted deletion of the T-bet gene and severe combined immunodeficient mice receiving CD4(+) cells from T-bet knockout mice spontaneously demonstrated multiple physiological and inflammatory features characteristic of asthma, Thus, T-bet deficiency, in the absence of allergen exposure, induces a murine phenotype reminiscent of both acute and chronic human asthma.