ArticleGut2004
Impairment of intestinal intraepithelial lymphocytes in Id2 deficient mice.
Article in Gut, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- Cross-tissue single-cell atlas reveals Id2 promotes sepsis-induced tissue damage by mediating macrophage metabolic reprogramming via Pkm2.International journal of biological sciences · 2026Article
- Unravelling butyrate metabolism in sepsis: identification of key genes.BMC infectious diseases · 2025Article
- Conserved developmental rewiring of the TCR signalosome drives tolerance in innate-like lymphocytes.bioRxiv : the preprint server for biology · 2025Article
- Inhibitor of Differentiation-2 Protein Ameliorates DSS-Induced Ulcerative Colitis by Inhibiting NF-κB Activation in Neutrophils.Frontiers in immunology · 2021Article
- Id2 Determines Intestinal Identity through Repression of the Foregut Transcription Factor Irx5.Molecular and cellular biology · 2018Article
- Impact of the gut microbiota on enhancer accessibility in gut intraepithelial lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Transcription factor networks directing the development, function, and evolution of innate lymphoid effectors.Annual review of immunology · 2015Review
- IL-7 and IL-15 independently program the differentiation of intestinal CD3-NKp46+ cell subsets from Id2-dependent precursors.The Journal of experimental medicine · 2010Article
- Surviving the crash: transitioning from effector to memory CD8+ T cell.Seminars in immunology · 2009Review
- Regulation of Id2 expression by CCAAT/enhancer binding protein beta.Nucleic acids research · 2005Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundId2, an inhibitor of basic helix-loop-helix transcription factors, regulates cell differentiation. Id2-/- mice exhibit a variety of phenotypes in the immune system.
aimsIn this study we investigated whether Id2 plays a role in intestinal intraepithelial lymphocytes (IELs), which constitute the main defence against pathogens in the intestinal tract.
methodsFlow cytometry and bone marrow transplantation were used to analyse and characterise subsets of IELs of Id2-/- mice. Gene expression was analysed by real-time polymerase chain reaction. Intestinal barrier function was evaluated by treating mice with 5-fluorouracil (5-FU).
resultsAmong the four members of the Id gene family, Id2 was selectively expressed in all T cell subsets in the small intestinal IELs. Id2-/- mice showed alteration in the proportions of T cell subsets and a substantial reduction in the number of IELs, especially those of the CD4+ and CD8 alpha beta+ T cell subsets, indicating a more pronounced effect on thymus derived IELs. Expression of alphaE integrin was reduced in CD4+ and CD8 alpha beta+ T cell subsets in IELs of Id2-/- mice. IELs isolated from C57BL/6 mice reconstituted with Id2-/- bone marrow cells showed a similar phenotype to that of Id2-/- mice, indicating that the defects are intrinsic to bone marrow derived cells. Expression of genes encoding intestinal epithelial cell derived cytokines was reduced in Id2-/- mice. The 5-FU treatment revealed impaired intestinal barrier function of Id2-/- mice.
conclusionsThe Id2 gene is essential for constituting the intestinal mucosal barrier, particularly with respect to IELs. Id2 null mutant mice may provide a good experimental model for studying the ontogeny of IELs and intestinal inflammation and infection.
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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.