Iron deficiency impairs Intra-hepatic lymphocyte mediated immune response
Open accessAbstract
Hepatic expression of iron homeostasis genes and serum iron parameters predict the success of immunosuppression withdrawal following clinical liver transplantation, a phenomenon known as spontaneous operational tolerance. In experimental animal models, spontaneous liver allograft tolerance is established through a process that requires intra-hepatic lymphocyte activation and deletion. Our aim was to determine if changes in systemic iron status regulate intra-hepatic lymphocyte responses. We used a murine model of lymphocyte-mediated acute liver inflammation induced by Concanavalin A (ConA) injection employing mice fed with an iron-deficient (IrDef) or an iron-balanced diet (IrRepl). While the mild iron deficiency induced by the IrDef diet did not significantly modify the steady state immune cell repertoire and systemic cytokine levels, it significantly dampened inflammatory liver damage after ConA challenge. These findings were associated with a marked decrease in T cell and NKT cell activation following ConA injection in IrDef mice. The decreased liver injury observed in IrDef mice was independent from changes in the gut microflora, and was replicated employing an iron specific chelator that did not modify intra-hepatic hepcidin secretion. Furthermore, low-dose iron chelation markedly impaired the activation of isolated T cells in vitro. All together, these results suggest that small changes in iron homeostasis can have a major effect in the regulation of intra-hepatic lymphocyte mediated responses.
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Levels of CD25 and phosphorylation of STAT5 are reduced upon iron chelation.
“In addition, levels of CD25 and phosphorylation of STAT5 are reduced upon iron chelation (Bonaccorsi-Riani et al., 2015; Zhang, 2020; Zhang et al. , 2018a,b,c).”
From Iron in infection and immunity (2020) · cites this paper as Bonaccorsi-Riani et al., 2015
The Results section ('Reduced iron availability impairs lymphocyte proliferation and activation'; page not provided) reports decreased CD25 expression in isolated CD4+ naïve T cells after iron chelation. Our copy does not report reduced STAT5 phosphorylation; a search for STAT5 phosphorylation found no supporting passage. (LLM, conf=0.88)
Experimental — accuracy not yet measuredIron chelation appears to directly inhibit expression of FoxP3, the master switch transcription factor of Tregs.
“Iron chelation appears to directly inhibit the expression of FoxP3, the master switch transcription factor of Tregs.”
From Iron in infection and immunity (2020) · cites this paper as Bonaccorsi-Riani et al., 2015
The Results section on reduced iron availability reports that chelation impaired T-cell proliferation and CD25 expression, but does not report FoxP3 expression after chelation. In the separate steady-state dietary iron-deficiency experiment, Foxp3 expression showed no significant change; that finding does not establish the effect of chelation. (LLM, conf=0.76)
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宋靜淑, Wu, Q., Green, D. R., Wang, F., & Min, J. (2026) · Nature reviews. Immunology · doi:10.1038/s41577-026-01337-8 · Cited by 1 · see citing works
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Modulation de l'activation des lymphocytes T et des réponses anti-tumorales par le fer
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- Authors
- Bonaccorsi-Riani, E., Danger, R., Lozano, J. J., Martinez-Picola, M., Kodela, E., Mas-Malavila, R., Bruguera, M., Collins, H. L., Hider, R. C., Martinez-Llordella, M., & Sanchez-Fueyo, A.
- Affiliations
- University of London (GB)
- Hospital Clínic de Barcelona (ES)
- King's College London (GB)
- Venue
- PLOS ONE
- Publisher
- Public Library of Science (PLoS)
- Published
- 2015-08-19
- Volume
- 10
- Issue
- 8
- Pages
- e0136106
- ISSN
- 1932-6203 (ISSN-L)
- PMC
- PMC4542211
- OpenAlex
- W1853633098
- Cited by
- 57
- References
- 37
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 3 · 2023: 8 · 2022: 10 · 2021: 4 · 2020: 6 · 2019: 2 · 2018: 6 · 2017: 4 · 2016: 6 · 2015: 1
- FWCI
- 4.45
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- PLoS ONE (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Research Portal (King's College London) (submittedVersion, cc-by)
- Funders
- National Institute for Health and Care Research (J006742/1)
- King's College London
- Medical Research Council (MR/L008890/1, J006742/1, MR/J006742/1)
- Menzies Centre for Australian Studies, King's College London, University of London
- Topics
- Health Sciences › Medicine › Hematology › Iron Metabolism and Disorders
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Hepatology › Liver physiology and pathology
- Keywords
- iron deficiency, iron homeostasis, liver transplantation, concanavalin A-induced liver injury, T cell activation, NKT cells, iron chelation, hepcidin, iron-deficient diet, liver inflammation
- MeSH terms
- Gastrointestinal Microbiome, Iron Deficiencies, Animals, Concanavalin A, Homeostasis, Liver, Lymphocyte Activation, Lymphocytes, Male, Mice, Inbred C57BL, T-Lymphocytes, Liver Transplantation, Cytokines, Cell Proliferation, Mice, Natural Killer T-Cells, Hepcidins
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