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Deregulated stress system in non-obese diabetic lymphocyte

Genes & Immunity volume 7, pages 352–358 (2006)Cite this article

Abstract

Lymphopenia-induced homeostatic expansion in non-obese diabetic (NOD) mice may lead to autoimmunity. We demonstrated that NOD lymphocytes are more susceptible to apoptosis than those of non-diabetic C57BL/6 or NOD.H2h4 mice in vivo and in vitro, which may be an underlying mechanism causing lymphopenia in NOD mice. Gene expression profiling identified a set of genes that are differentially expressed between NOD and B6 mice. Identity of these genes suggested that NOD T cells have a deregulated stress response system, especially heat-shock protein family, making them overly sensitive to apoptosis. Thus, we hypothesize that this strain-specific gene expression profile may confer a liability upon NOD T cells making them more susceptible to apoptosis that may lead to lymphopenia in NOD mice and contribute to development of autoimmunity.

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Acknowledgements

This work was supported by National Institutes of Health Grant DK 58765. The Vanderbilt Microarray Shared Resource is supported by the Vanderbilt Ingram Cancer Center (P30 CA68485), the Vanderbilt Diabetes Research and Training Center (P60 DK20593) and the Vanderbilt Digestive Disease Center (P30 DK58404).

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Authors and Affiliations

  1. Department of Medicine, Division of Rheumatology, Vanderbilt University School of Medicine, Nashville, TN, USA

    Z Liu & T M Aune

  2. Department of Microbiology and Immunology, Vanderbilt University School of Medicine, Nashville, TN, USA

    Z Liu & T M Aune

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  1. Z Liu
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  2. T M Aune
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Correspondence to T M Aune.

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Liu, Z., Aune, T. Deregulated stress system in non-obese diabetic lymphocyte. Genes Immun 7, 352–358 (2006). https://doi.org/10.1038/sj.gene.6364306

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  • DOI: https://doi.org/10.1038/sj.gene.6364306

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