ArticleJournal of immunology (Baltimore, Md. : 1950)2008
Cutting edge: the Idd3 genetic interval determines regulatory T cell function through CD11b+CD11c- APC.
Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 21 citations in OpenAlex.
- Characterization of γδT cells in lung of Plasmodium yoelii-infected C57BL/6 mice.Malaria journal · 2021Article
- Reduced interleukin-2 responsiveness impairs the ability of Treg cells to compete for IL-2 in nonobese diabetic mice.Immunology and cell biology · 2016Article
- Non-classical MHC I-E negatively regulates macrophage activation and Th17 cell development in NOD mice.Scientific reports · 2015Article
- A T cell extrinsic mechanism by which IL-2 dampens Th17 differentiation.Journal of autoimmunity · 2015Article
- EFFECT OF LIPOSOMAL CLODRONATE-DEPENDENT DEPLETION OF PROFESSIONAL ANTIGEN PRESENTING CELLS ON NUMBERS AND PHENOTYPE OF CANINE CD4+CD25+FOXP3+ REGULATORY T CELLS.Journal of veterinary medicine and research · 2014Article
- Blockade of the programmed death-1 (PD1) pathway undermines potent genetic protection from type 1 diabetes.PloS one · 2014Article
- Dendritic cell subsets in type 1 diabetes: friend or foe?Frontiers in immunology · 2013Review
- Immunomodulation of antigen presenting cells promotes natural regulatory T cells that prevent autoimmune diabetes in NOD mice.PloS one · 2012Article
- Differential IL-21 signaling in APCs leads to disparate Th17 differentiation in diabetes-susceptible NOD and diabetes-resistant NOD.Idd3 mice.The Journal of clinical investigation · 2011Article
- Reduced IL-2 expression in NOD mice leads to a temporal increase in CD62Llo FoxP3+ CD4+ T cells with limited suppressor activity.European journal of immunology · 2011Article
- Mouse models for the study of autoimmune type 1 diabetes: a NOD to similarities and differences to human disease.Seminars in immunopathology · 2011Review
- Nonobese diabetic congenic strain analysis of autoimmune diabetes reveals genetic complexity of the Idd18 locus and identifies Vav3 as a candidate gene.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- Expression of diabetes-associated genes by dendritic cells and CD4 T cells drives the loss of tolerance in nonobese diabetic mice.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The Idd3 genetic interval confers protection against multiple autoimmune diseases, including type 1 diabetes and experimental autoimmune encephalomyelitis. The favored candidate gene in this interval is Il2, which is polymorphic between susceptible and resistant strains of mice. IL-2 regulates the growth/death of effector T cells as well as the generation/maintenance of regulatory T cells (Tregs), and recent studies have shown that NOD.Idd3 Tregs are more suppressive than their NOD counterparts. We have further dissected the mechanisms underlying the differential suppression by NOD and NODxIdd3 Tregs and find that it is determined by CD11b(+)CD11c(-) APCs. Thus, contrary to what might be expected, our data suggest that the differential suppressive activity of NOD and NODxIdd3 Tregs is not due to an effect of the Idd3 genetic interval on T cells but rather is due to differences in the APC compartment.
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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.