Pancreatic Lymph Node-Derived CD4+CD25+ Treg Cells
Open accessAbstract
Inflammation can activate self-reactive CD8(+) T cells and induce autoimmunity. Here we show in a CD8(+) T cell-mediated model of type 1 diabetes that CD4(+)CD25(+) Treg cells prevent beta cell destruction following localized inflammation in the islets of Langerhans. These Treg cells accumulate preferentially in the pancreatic lymph nodes and islets but not other lymph nodes or spleen. PLN-derived Treg cells are extremely potent; only 2 x 10(3) cells are needed to prevent diabetes development, and their capacity to regulate is dependent on TNF-related activation induced cytokine-receptor activator of NFkappaB signals. Indeed, blockade of this pathway results in decreased frequency of CD4(+)CD25(+) Treg cells in the PLN, resulting in intra-islet differentiation of CD8(+) T cells into CTLs and rapid progression to diabetes.
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In a mouse study, the number of sunburn cells was decreased and DNA fragmentation was reduced in proportion to the UVA/UVB ratio.
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From Molecular Mechanisms of UV-Induced Apoptosis and Its Effects on Skin Residential Cells: The Implication in UV-Based Phototherapy (2013) · cites this paper as [24]
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Self-citation
- Authors
- Green, E. A., Choi, Y., & Flavell, R. A.
- Affiliations
- University of Cambridge (GB)
- University of Pennsylvania (US)
- Howard Hughes Medical Institute (US)
- Corresponding author
- Flavell, Richard A
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2002-02
- Volume
- 16
- Issue
- 2
- Pages
- 183-191
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2028421750
- Cited by
- 310
- References
- 0
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 4 · 2023: 4 · 2022: 9 · 2021: 5 · 2020: 8 · 2019: 3 · 2018: 7 · 2017: 8 · 2016: 9 · 2015: 5 · 2014: 6 · 2013: 8 · 2012: 7
- FWCI
- 11.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 4184 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health
- Juvenile Diabetes Research Foundation United States of America
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Diabetes and associated disorders
- Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
- Keywords
- regulatory T cells, CD4+CD25+ Treg, pancreatic lymph nodes, type 1 diabetes, beta cell destruction, insulitis, RANKL, RANK, RANK/RANKL signaling, islet autoimmunity
- MeSH terms
- Animals, Carrier Proteins, Cell Differentiation, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 1, Disease Models, Animal, Female, Glycoproteins, Islets of Langerhans, Ligands, Lymph Nodes, Male, Membrane Glycoproteins, Mice, Inbred C57BL, Mice, Transgenic, Pancreas, T-Lymphocytes, Cytotoxic, Receptors, Interleukin-2, Signal Transduction, Biomarkers, CD4-Positive T-Lymphocytes, Receptors, Tumor Necrosis Factor, Receptors, Cytoplasmic and Nuclear, CD8-Positive T-Lymphocytes, Mice, Osteoprotegerin, RANK Ligand, Receptor Activator of Nuclear Factor-kappa B
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