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Wientjens et al (Immunity 2025 Dec 10:S1074-7613(25)00520-5; https://doi.org/10.1016/j.immuni.2025.11.018) identified a critical role for the nonessential amino acid cystine in pathogenic group 2 innate lymphoid cells (ILC2s) responses in mice. More specifically, expansion of pathogenic ILC2s during allergic airway inflammation required cystine to synthesize glutathione, which acted in concert with glutathione peroxidase 4 (GPX4) and thioredoxin reductase 1 (TXNRD1) to prevent ferroptosis, which is a regulated cell death pathway marked by iron accumulation, lipid peroxidation, and induction of reactive oxygen species.

Publication Details

Journal
Journal of Allergy and Clinical Immunology
Published
2026-04-01
DOI
https://doi.org/10.1016/j.jaci.2026.02.015
Primary Topic
IL-33, ST2, and ILC Pathways
Type
article
Field-Weighted Citation Impact
0.00
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News beyond our pages

Journal of Allergy and Clinical Immunology
IL-33, ST2, and ILC Pathways
article

News beyond our pages

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Abstract

Wientjens et al (Immunity 2025 Dec 10:S1074-7613(25)00520-5; https://doi.org/10.1016/j.immuni.2025.11.018) identified a critical role for the nonessential amino acid cystine in pathogenic group 2 innate lymphoid cells (ILC2s) responses in mice. More specifically, expansion of pathogenic ILC2s during allergic airway inflammation required cystine to synthesize glutathione, which acted in concert with glutathione peroxidase 4 (GPX4) and thioredoxin reductase 1 (TXNRD1) to prevent ferroptosis, which is a regulated cell death pathway marked by iron accumulation, lipid peroxidation, and induction of reactive oxygen species.

Journal of Allergy and Clinical ImmunologyVol. 157(4)
Openalex Percentile: Top 8%
IL-33, ST2, and ILC Pathways
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News beyond our pages · Journal of Allergy and Clinical Immunology (2026) | TGRS Research Map | TGRS