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Innate lymphoid cells at the interface between obesity and asthma
Author(s) -
Everaere Laetitia,
Ait Yahia Saliha,
Bouté Mélodie,
Audousset Camille,
Chenivesse Cécile,
Tsicopoulos Anne
Publication year - 2018
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.12832
Subject(s) - innate lymphoid cell , asthma , immunology , obesity , transcription factor , biology , disease , cytokine , medicine , innate immune system , immune system , endocrinology , genetics , gene
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.