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首页> 外文期刊>Immunology: An Official Journal of the British Society for Immunology >Innate lymphoid cells at the interface between obesity and asthma
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Innate lymphoid cells at the interface between obesity and asthma

机译：在肥胖和哮喘之间的界面处先天淋巴细胞

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Summary Obesity and asthma prevalence has dramatically and concomitantly increased over the last 25 years, and many epidemiological studies have highlighted obesity as an important risk factor for asthma. Although many studies have been performed, the underlying mechanisms remain poorly understood. Innate mechanisms have been involved in both diseases, in particular through the recently described innate lymphoid cells ( ILC s). ILC s are subdivided into three groups that are defined by their cytokine production and by their master transcription factor expression, in sharp correlation with their T helper counterparts. However, unlike T helper cells, ILC s do not express antigen‐specific receptors, but respond to damage‐induced signals. ILC s have been found in target tissues of both diseases, and data have implicated these cells in the pathogenesis of both diseases. In particular group 2 ILC s ( ILC 2) are activated in both the adipose and lung tissues under the effect of interleukin‐33 and interleukin‐25 expression. However, counter‐intuitively to the well‐known association between obesity and asthma, ILC 2 are beneficial for obesity but deleterious for asthma. This review will examine the roles of ILC s in each disease and recent data highlighting ILC s as a putative link between obesity and asthma.
机译：摘要肥胖和哮喘患病率在过去25年中大大增加，并且许多流行病学研究突出了肥胖症作为哮喘的重要危险因素。虽然已经进行了许多研究，但潜在的机制仍然明白很差。先天机制已经参与了这两种疾病，特别是通过最近描述的先天淋巴细胞（ILC S）。 ILC S细分为三组，其由其细胞因子产生和母体转录因子表达定义，与其T辅助对应物的急剧相关。然而，与T辅助细胞不同，ILC S不表达抗原特异性受体，但响应损伤诱导的信号。 ILC S已被发现在两种疾病的靶组织中，并且数据在两种疾病的发病机制中暗示了这些细胞。特别是，在白细胞介素-33和白细胞介素-25表达的作用下，2，ILC S（ILC 2）在脂肪和肺组织中被激活。然而，反向直观地对肥胖症和哮喘之间的众所周知的关联，ILC 2对肥胖而对哮喘有害，对哮喘有害。该审查将研究ILC S在每种疾病中的角色和最近突出ILC S作为肥胖和哮喘之间的推定联系。

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