The DOI matches its Crossref record; 70 of the 70 references it cites were found in a registry or an index.
Reprogramming of CTLs into natural killer–like cells in celiac disease
Open accessAbstract
Celiac disease is an intestinal inflammatory disorder induced by dietary gluten in genetically susceptible individuals. The mechanisms underlying the massive expansion of interferon γ–producing intraepithelial cytotoxic T lymphocytes (CTLs) and the destruction of the epithelial cells lining the small intestine of celiac patients have remained elusive. We report massive oligoclonal expansions of intraepithelial CTLs that exhibit a profound genetic reprogramming of natural killer (NK) functions. These CTLs aberrantly expressed cytolytic NK lineage receptors, such as NKG2C, NKp44, and NKp46, which associate with adaptor molecules bearing immunoreceptor tyrosine-based activation motifs and induce ZAP-70 phosphorylation, cytokine secretion, and proliferation independently of T cell receptor signaling. This NK transformation of CTLs may underlie both the self-perpetuating, gluten-independent tissue damage and the uncontrolled CTL expansion leading to malignant lymphomas in severe forms of celiac disease. Because similar changes were detected in a subset of CTLs from cytomegalovirus-seropositive patients, we suggest that a stepwise transformation of CTLs into NK-like cells may underlie immunopathology in various chronic infectious and inflammatory diseases.
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“Under stress or inflammatory conditions, such as in celiac disease, iIELs upregulate the expression of activating NKG2D and CD94/NKG2C receptors, (which recognize MICA/B and HLA-E, respectively) while losing the expression of the inhibitory receptors CD94/NKG2A [302, 306-308].”
From Guidelines for the use of flow cytometry and cell sorting in immunological studies (third edition) (2021) · cites this paper as [306]
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Cites
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HLA-E binds to natural killer cell receptors CD94/NKG2A, B and C
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Self-citationHLA-E is a major ligand for the natural killer inhibitory receptor CD94/NKG2A
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Self-citationInterleukin 15: biology and relevance to human disease
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Coeliac disease: dissecting a complex inflammatory disorder
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Flagged first, then by citations
Research works printed but not linked: 4
- 2006, Curr. Top. Microbiol. Immunol., 298, 139
- 2004, Blood., 104, 3664
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- 2005, Nucleic Acids Res., 33, D593
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Items 301–322 of 322
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Cheng, L., Bianchi, N., Soldati, H., Bersier, L., Evrard, M., Caillon, A., Chawla, A. S., Nakken, B., Szodoray, P., Bousser, E. D., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.01.02.697332 · Cited by 1
Mandile, R., Discepolo, V., Auricchio, R., & Troncone, R. (2026) · Gastroenterology · doi:10.1053/j.gastro.2026.03.005
Rôle des lymphocytes cytotoxiques dans les hypersensibilités retardées cutanées
Nosbaum, A. (2013) · theses.fr (ABES) · doi:10.70675/08df0469z5fdbz4f7bz9dbdz857258a2c88d
Acquisition and regulation of effector T cell functions in Crohn’s disease
Bottois, H. (2019) · theses.fr (ABES) · doi:10.70675/5f587a4azaf7ez4b0dz8e72z4739bce7ff73
Etude des mécanismes de régulation de l'activation des cellules natural killer
Guia, S. (2021) · theses.fr (ABES) · doi:10.70675/fe8a748dzb006z40a0z8e07z1043717cbdd0
Ferron, E. (2024) · theses.fr (ABES) · doi:10.70675/f7ee5cbez3975z4d1fz908cz5a84a3a5f736
Etude des mécanismes de contrôle des cellules tumorales par les cellules Natural Killer
Fenis, A. (2024) · theses.fr (ABES) · doi:10.70675/747c59caz7a79z4064z989cz9dd2bc8bd27e
Resendiz, A. O. (2023) · theses.fr (ABES) · doi:10.70675/a581f48bzaf00z4878zaa50z4d7b68e7d45d
Guégan, N. (2024) · theses.fr (ABES) · doi:10.70675/ec31ff94zb0e6z403ez9f71zfa026392bcb2
Development of a protocol to produce Natural Killer cells for therapeutic purposes
Corredera, M. M. (2024) · theses.fr (ABES) · doi:10.70675/f1f1aec4zc7efz49d1z9111z30fce374ad41
Multiscale Kinetic Model for Immune Reaction in Coeliac Disease
Burini, D., Knopoff, D. A., & Serrano, L. (2026) · Mathematics · doi:10.3390/math14081333
Resendiz, A. O., Petitdemange, C., Lazzerini, M., Jacquelin, B., Beaumont, E., Perdomo-Celis, F., Samri, A., Lambotte, O., Meyer, L., Goujard, C., et al. (2026) · Med · doi:10.1016/j.medj.2026.101143
Li, T. M., & Edelblum, K. L. (2026) · Elsevier eBooks · doi:10.1016/b978-0-443-40306-4.00008-9
Protocolo para el diagnóstico precoz de la enfermedad celíaca. Actualización
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Adaptive-like features of the γδ TCR couple chronic BTNL recognition to NK-like tissue immunityPreprint
McDonald, B. D., Anderson, H. D., Mayassi, T., Sok, C. L., Locher, V., Justyniarska, M., Borregard, M., Kaiser, C., Ladell, K., McLaren, J. E., et al. (2026) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.64898/2026.09.17.751481
Detection and control of gluten as a food allergen
Nasr, I. H., Messing, J. W., Nasr, I. H., & Ciclitira, P. J. (2014) · Elsevier eBooks · doi:10.1533/9781782420217.3.367
Metadata
- Authors
- Meresse, B., Curran, S. A., Ciszewski, C., Orbelyan, G., Setty, M., Bhagat, G., Lee, L., Tretiakova, M., Semrad, C., Kistner, E., Winchester, R. J., Braud, V., Lanier, L. L., Geraghty, D. E., Green, P. H., Guandalini, S., & Jabri, B.
- Affiliations
- 1Department of Pathology,
- 2Department of Pediatrics,
- 6Department of Pathology, and
- 3Department of Medicine, and
- University of Chicago (US)
- 5Division of Autoimmune and Molecular Diseases,
- 8Institut de Pharmacologie Moleculaire et Cellulaire, Centre National de la Recherche Scientifique/Université de Nice-Sophia Antipolis, UMR6097, 06560 Valbonne, France
- University of California, San Francisco (US)
- Fred Hutch Cancer Center (US)
- Columbia University (US)
- ORCID
- Venue
- The Journal of Experimental Medicine
- Publisher
- Rockefeller University Press
- Published
- 2006-05-08
- Volume
- 203
- Issue
- 5
- Pages
- 1343-1355
- ISSN
- 0022-1007 (ISSN-L)
- 1540-9538
- PMC
- PMC2121214
- OpenAlex
- W2128452798
- Cited by
- 322
- References
- 68
- Citations by year
- 2026: 8 · 2025: 12 · 2024: 22 · 2023: 13 · 2022: 10 · 2021: 27 · 2020: 16 · 2019: 13 · 2018: 12 · 2017: 12 · 2016: 13 · 2015: 14 · 2014: 15 · 2013: 16 · 2012: 16
- FWCI
- 21.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Experimental Medicine (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion, cc-by-nc-sa)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Cancer Institute (R01 CA89294, R01CA089294)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK058727, R01DK58727, R01DK063158)
- Topics
- Health Sciences › Medicine › Gastroenterology › Celiac Disease Research and Management
- Life Sciences › Immunology and Microbiology › Immunology › Immune Cell Function and Interaction
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Keywords
- celiac disease, cytotoxic T lymphocytes, NKG2C, NKp44, NKp46, ZAP-70, interferon-gamma, intraepithelial lymphocytes, cytomegalovirus, lymphoma, intestinal epithelial damage, chronic inflammation, immunopathology
- MeSH terms
- Base Sequence, Celiac Disease, Cell Differentiation, Chronic Disease, Cytomegalovirus Infections, Gene Expression Regulation, Humans, Interferon-gamma, Intestinal Mucosa, Intestine, Small, Killer Cells, Natural, Lymphoma, Molecular Sequence Data, Phosphorylation, Protein Processing, Post-Translational, Receptors, Immunologic, T-Lymphocytes, Cytotoxic, Signal Transduction, Gene Expression Profiling, Cell Proliferation, ZAP-70 Protein-Tyrosine Kinase
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