Increased thymic development of regulatory T cells in NOD mice is functionally dissociated from type I diabetes susceptibility. Issue 5 (11th March 2013)

• Record Type: Journal Article
• Authors: Tellier, Julie; Andrianjaka, Andry; Vicente, Rita; Thiault, Nicolas; Enault, Geneviève; Garchon, Henri‐Jean; van Meerwijk, Joost P. M.; Romagnoli, Paola
• Is Part Of: European journal of immunology. Volume 43:Issue 5(2013:May)
• Page Start: 1356
• Page End: 1362
• Publication Date: 2013-03-11
• Subjects: Immunology -- Periodicals; 616.079
• DOI: 10.1002/eji.201243142
• Languages: English
• ISSNs: 0014-2980

Abstract

<abstract abstract-type="main"> <title> <x xml:space="preserve">Abstract</x> </title> <p>Regulatory T (Treg) lymphocytes play a central role in the control of autoimmune pathology. Any alteration in Treg‐cell biology in mouse strains used for the study of these disorders therefore raises the question of its direct link with disease susceptibility. Paradoxically, in non‐obese diabetic (NOD) mice increased numbers of Treg cells develop in the thymus. In this report we identify a locus of &lt;7 Mbp that quantitatively controls Treg‐cell development in the thymus of the NOD mouse. This '<italic>Trd1</italic>' region is located centromeric to the <italic>H2</italic> complex on chromosome 17 and does not include genes encoding classical MHC molecules. The genomic region identified here contains the <italic>Idd16</italic> diabetes susceptibility locus and the use of congenic mouse strains allowed us to investigate the potential link between quantitatively altered thymic Treg cells and diabetes susceptibility. Hybrid mice present similar levels of thymic Treg cells as B6 animals but they developed diabetes with the same kinetics as NOD mice. Therefore, the increased Treg‐cell development in NOD mice controlled by <italic>Trd1</italic> is functionally dissociated from the susceptibility of NOD to diabetes.</p> </abstract>