ArticleMucosal immunology2022
Bilirubin represents a negative regulator of ILC2 in allergic airway inflammation.
Article in Mucosal immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 18 citations in OpenAlex.
- A Comprehensive Review of Natural Products Against Allergic Rhinitis and Asthma: From Sensitization to Chronic Remodeling.International journal of molecular sciences · 2026Review
- Bilirubin Alleviates Spinal Cord Injury by Enhancing SOCS3-Mediated Anti-Inflammatory Effects via Gas6-Axl Signaling.CNS neuroscience & therapeutics · 2025Article
- Bilirubin Targeting WNK1 to Alleviate NLRP3-Mediated Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Extracellular vesicles derived from lung M2 macrophages enhance group 2 innate lymphoid cells function in allergic airway inflammation.Experimental & molecular medicine · 2025Article
- One Year of Oral Immunotherapy Impacts the Gut Microbiota and Plasma Metabolome of Peanut-Allergic Young Children.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2025Article
- E3 ligase RNF128 restricts A. alternata-induced ILC2 activation and type 2 immune response in the murine lung.Scientific reports · 2025Article
- Toward nanotechnology-enabled application of bilirubin in the treatment and diagnosis of various civilization diseases.Materials today. Bio · 2023Review
- Clinical Utility of the Neutrophil-to-Bilirubin Ratio in the Detection of Disease Activity in Ulcerative Colitis.Journal of inflammation research · 2023Article
- CD90 is not constitutively expressed in functional innate lymphoid cells.Frontiers in immunology · 2023Article
- Heterogeneity of type 2 innate lymphoid cells.Nature reviews. Immunology · 2022Review
- Immune Regulation of Heme Oxygenase-1 in Allergic Airway Inflammation.Antioxidants (Basel, Switzerland) · 2022Review
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Authors and funding
14 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Group 2 innate lymphoid cells (ILC2s) play an important role in allergic airway inflammation. Despite recent advances in defining molecular mechanisms that control ILC2 development and function, the role of endogenous metabolites in the regulation of ILC2s remains poorly understood. Herein, we demonstrated that bilirubin, an end product of heme catabolism, was a potent negative regulator of ILC2s. Bilirubin metabolism was found to be significantly induced during airway inflammation in mouse models. The administration of unconjugated bilirubin (UCB) dramatically suppressed ILC2 responses to interleukin (IL)-33 in mice, including cell proliferation and the production of effector cytokines. Furthermore, UCB significantly alleviated ILC2-driven airway inflammation, which was aggravated upon clearance of endogenous UCB. Mechanistic studies showed that the effects of bilirubin on ILC2s were associated with downregulation of ERK phosphorylation and GATA3 expression. Clinically, newborns with hyperbilirubinemia displayed significantly lower levels of ILC2 with impaired function and suppressed ERK signaling. Together, these findings indicate that bilirubin serves as an endogenous suppressor of ILC2s and might have potential therapeutic value in the treatment of allergic airway inflammation.
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