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Low rate of proliferation in immature thymocytes of the non-obese diabetic mouse maps to the Idd6 diabetes susceptibility region
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department of Cell and Molecular Biology, Umeå University, Umeå, Sweden)
Gulbenkian Institute for Science, Oeiras, Portugal, PT.
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department of Cell and Molecular Biology. University of Umeå)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department of Cell and Molecular Biology. University of Umeå)
2001 (English)In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 44, no 8, 1054-1061 p.Article in journal (Refereed) Published
Abstract [en]

AIMS/HYPOTHESIS: The non-obese diabetic (NOD) mouse spontaneously develops T-cell-dependent autoimmune diabetes. This mouse strain has a number of immune dysfunctions related to T-cell development but so far there are no available data on the proliferation of NOD immature thymocytes. We therefore studied the thymocyte proliferation in the NOD mouse in discrete stages of T-cell development.

METHODS: We depleted thymocytes in vivo and analysed thymocyte proliferation during the thymus recovery from depletion. We used co-segregation analysis and quantitative loci trait analysis to investigate the genetic control of proliferation impairments in NOD thymocytes.

RESULTS: Immature thymocytes of female NOD mice proliferate with a relatively low rate compared to non-autoimmune C57Bl/6 mice. This aberrant proliferation was most pronounced in CD4-/lo CD8+ cells differentiating from the CD4-CD8- to the CD4+CD8+ stage. A genetic mapping study using an F2 intercross between the NOD and the C57BL/6 strains showed that a major locus controlling this trait is linked to the insulin-dependent diabetes susceptibility locus Idd6.

CONCLUSION/INTERPRETATION: Our results suggest that impairment of proliferation of immature thymocytes is one possible mechanism through which the Idd6 locus contributes to the pathogenesis of diabetes.

Place, publisher, year, edition, pages
Springer, 2001. Vol. 44, no 8, 1054-1061 p.
National Category
Basic Medicine
Research subject
Immunology
Identifiers
URN: urn:nbn:se:umu:diva-87518DOI: 10.1007/s001250100600PubMedID: 11484085OAI: oai:DiVA.org:umu-87518DiVA: diva2:709626
Available from: 2014-04-02 Created: 2014-04-02 Last updated: 2017-12-05Bibliographically approved

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Bergman, Marie-LouiseLejon, KristinaHolmberg, Dan
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