ReviewFrontiers in immunology2026
The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Respiratory diseases represent a major global public health burden, and type 2 immunity plays a key role in their pathogenesis. The interleukin-33 (IL-33)-group 2 innate lymphoid cell (ILC2) axis regulates airway type 2 immune responses, thereby triggering, amplifying, and maintaining pathological inflammation. This review addresses the characteristics of IL-33 and pulmonary ILC2s, including the alarmin function and tissue-specific expression of IL-33, and the origin, localization, functional heterogeneity, and microenvironment-driven plasticity of ILC2s. In particular, we discuss how disease-specific microenvironments shape divergent ILC2 states, including classical type 2 cytokine-producing ILC2s, tissue-repairing AREG-producing ILC2s, ILC1-like cells, and IL-17-producing ILC2-like states. We further review the regulatory mechanisms of the IL-33-ILC2 axis in bronchopulmonary dysplasia, asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and viral respiratory infections are also discussed, highlighting the remarkable functional plasticity of ILC2s. Targeting the IL-33-ILC2 axis and modulating ILC2 function represent therapeutic strategies for various type 2-mediated airway diseases.
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