ArticleThe Journal of experimental medicine2023
The cIAP ubiquitin ligases sustain type 3 γδ T cells and ILC during aging to promote barrier immunity.
Article in The Journal of experimental medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Crosstalk between the microbiota and intestinal γδ T cell compartments in health and IBD.Gut microbes · 2026Review
- A temporal differentiation program after birth delineates γδ T cell immunity.Science advances · 2026Article
- Identification of ubiquitination-related signature genes for predicting kidney transplant rejection.Scientific reports · 2026Article
- Intestinal aging-related immune dysfunction: mechanisms and interventions.Acta biochimica et biophysica Sinica · 2026Review
- GFI1 as a novel regulator of γδ T cell development and the IL-17/IFN-γ lineage commitment.Frontiers in immunology · 2026Article
- CAR-γδ T Cells Targeting Claudin18.2 Show Superior Cytotoxicity Against Solid Tumor Compared to Traditional CAR-αβ T Cells.Cancers · 2025Article
- Genomic deletion of Bcl6 differentially affects conventional dendritic cell subsets and compromises Tfh/Tfr/Th17 cell responses.Nature communications · 2024Article
- Understanding Type 3 Innate Lymphoid Cells and Crosstalk with the Microbiota: A Skin Connection.International journal of molecular sciences · 2024Review
- Innate lymphoid cells-Underexplored guardians of immunity.PLoS pathogens · 2023Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Early-life cues shape the immune system during adulthood. However, early-life signaling pathways and their temporal functions are not well understood. Herein, we demonstrate that the cellular inhibitor of apoptosis proteins 1 and 2 (cIAP1/2), which are E3 ubiquitin ligases, sustain interleukin (IL)-17-producing γ δ T cells (γδT17) and group 3 innate lymphoid cells (ILC3) during late neonatal and prepubescent life. We show that cell-intrinsic deficiency of cIAP1/2 at 3-4 wk of life leads to downregulation of the transcription factors cMAF and RORγt and failure to enter the cell cycle, followed by progressive loss of γδT17 cells and ILC3 during aging. Mice deficient in cIAP1/2 have severely reduced γδT17 cells and ILC3, present with suboptimal γδT17 responses in the skin, lack intestinal isolated lymphoid follicles, and cannot control intestinal bacterial infection. Mechanistically, these effects appear to be dependent on overt activation of the non-canonical NF-κB pathway. Our data identify cIAP1/2 as early-life molecular switches that establish effective type 3 immunity during aging.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.