ILC2s: team players in regulating asthma
Publication details: 2021-04-26.Subject(s): Genre/Form: Online resources: Summary: Type-2 immunity helps protect the host from infection, but also plays key roles in tissue homeostasis, metabolism and repair. Unfortunately, inappropriate type-2 immune reactions may lead to allergy and asthma. Group-2 innate lymphoid cells (ILC2s) in the lungs respond rapidly to local environmental cues, such as the release of epithelium-derived type-2 initiator cytokines/alarmins, producing type-2 effector cytokines such as IL-4, IL-5 and IL-13 in response to tissue damage and infection. ILC2s are associated with the severity of allergic asthma and experimental models of lung inflammation have shown how they act as playmakers, receiving signals variously from stromal and immune cells as well as the nervous system, and then disseminating cytokine cues to elicit effector functions and potentiate CD4+ T helper cell activation that characterise the pathology of allergic asthma. Recent breakthroughs identifying stromal and neuronal-derived microenvironmental cues that regulate ILC2s, along with studies recognizing the potential plasticity of ILC2s, have improved our understanding of the immunoregulation of asthma and opened new avenues for drug discovery./pmc/articles/PMC7614118/
/pubmed/33534604
Type-2 immunity helps protect the host from infection, but also plays key roles in tissue homeostasis, metabolism and repair. Unfortunately, inappropriate type-2 immune reactions may lead to allergy and asthma. Group-2 innate lymphoid cells (ILC2s) in the lungs respond rapidly to local environmental cues, such as the release of epithelium-derived type-2 initiator cytokines/alarmins, producing type-2 effector cytokines such as IL-4, IL-5 and IL-13 in response to tissue damage and infection. ILC2s are associated with the severity of allergic asthma and experimental models of lung inflammation have shown how they act as playmakers, receiving signals variously from stromal and immune cells as well as the nervous system, and then disseminating cytokine cues to elicit effector functions and potentiate CD4+ T helper cell activation that characterise the pathology of allergic asthma. Recent breakthroughs identifying stromal and neuronal-derived microenvironmental cues that regulate ILC2s, along with studies recognizing the potential plasticity of ILC2s, have improved our understanding of the immunoregulation of asthma and opened new avenues for drug discovery.
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