ArticleThe Journal of experimental medicine2012
Inducible colitis-associated glycome capable of stimulating the proliferation of memory CD4+ T cells.
Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
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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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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Immunological synapse: structures, molecular mechanisms and therapeutic implications in disease.Signal transduction and targeted therapy · 2025Review
- Glycosylation: mechanisms, biological functions and clinical implications.Signal transduction and targeted therapy · 2024Review
- Extracellular Galectin 4 Drives Immune Evasion and Promotes T-cell Apoptosis in Pancreatic Cancer.Cancer immunology research · 2023Article
- Galectin functions in cancer-associated inflammation and thrombosis.Frontiers in cardiovascular medicine · 2023Review
- Galectin network in osteoarthritis: galectin-4 programs a pathogenic signature of gene and effector expression in human chondrocytes in vitro.Histochemistry and cell biology · 2022Article
- Pretreatment with IPA ameliorates colitis in mice: Colon transcriptome and fecal 16S amplicon profiling.Frontiers in immunology · 2022Article
- Identification of Biomarkers Associated With CD4Frontiers in immunology · 2022Article
- Control of intestinal inflammation by glycosylation-dependent lectin-driven immunoregulatory circuits.Science advances · 2021Article
- Spatiotemporal regulation of galectin-1-induced T-cell death in lamina propria from Crohn's disease and ulcerative colitis patients.Apoptosis : an international journal on programmed cell death · 2021Article
- Mucin-Type O-Glycans: Barrier, Microbiota, and Immune Anchors in Inflammatory Bowel Disease.Journal of inflammation research · 2021Review
- Sweetening the hallmarks of cancer: Galectins as multifunctional mediators of tumor progression.The Journal of experimental medicine · 2020Review
- Breaking the Glyco-Code of HIV Persistence and Immunopathogenesis.Current HIV/AIDS reports · 2019Review
- The Modulatory Roles of N-glycans in T-Cell-Mediated Autoimmune Diseases.International journal of molecular sciences · 2018Review
- Galectins in Intestinal Inflammation: Galectin-1 Expression Delineates Response to Treatment in Celiac Disease Patients.Frontiers in immunology · 2018Article
- Expression of human cathelicidin peptide LL-37 in inflammatory bowel disease.Clinical and experimental immunology · 2018Article
- Expression of Interleukin-26 is upregulated in inflammatory bowel disease.World journal of gastroenterology · 2017Article
- The role of galectin-4 in physiology and diseases.Protein & cell · 2016Review
- Immunohistochemical Studies on Galectin Expression in Colectomised Patients with Ulcerative Colitis.BioMed research international · 2016Article
- Article
- Innate immunity against molecular mimicry: Examining galectin-mediated antimicrobial activity.BioEssays : news and reviews in molecular, cellular and developmental biology · 2015Review
Corrections and comments
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Authors and funding
15 authors at 8 institutions in 2 countries.
Funding
Abstract
Immune responses are modified by a diverse and abundant repertoire of carbohydrate structures on the cell surface, which is known as the glycome. In this study, we propose that a unique glycome that can be identified through the binding of galectin-4 is created on local, but not systemic, memory CD4+ T cells under diverse intestinal inflammatory conditions, but not in the healthy state. The colitis-associated glycome (CAG) represents an immature core 1-expressing O-glycan. Development of CAG may be mediated by down-regulation of the expression of core-2 β1,6-N-acetylglucosaminyltransferase (C2GnT) 1, a key enzyme responsible for the production of core-2 O-glycan branch through addition of N-acetylglucosamine (GlcNAc) to a core-1 O-glycan structure. Mechanistically, the CAG seems to contribute to super raft formation associated with the immunological synapse on colonic memory CD4+ T cells and to the consequent stabilization of protein kinase C θ activation, resulting in the stimulation of memory CD4+ T cell expansion in the inflamed intestine. Functionally, CAG-mediated CD4+ T cell expansion contributes to the exacerbation of T cell-mediated experimental intestinal inflammations. Therefore, the CAG may be an attractive therapeutic target to specifically suppress the expansion of effector memory CD4+ T cells in intestinal inflammation such as that seen in inflammatory bowel disease.
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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.