Deregulated stress system in non-obese diabetic lymphocyte.

Liu Z, Aune TM
Genes Immun. 2006 7 (5): 352-8

PMID: 16691184 · DOI:10.1038/sj.gene.6364306

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.H2(h4) 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.

MeSH Terms (20)

Animals Apoptosis Autoimmunity Bone Marrow Transplantation Cells, Cultured Diabetes Mellitus, Experimental DNA, Complementary Female Gamma Rays Gene Expression Profiling Heat-Shock Response Mice Mice, Inbred C57BL Mice, Inbred NOD Mice, Inbred Strains Spleen T-Lymphocytes T-Lymphocyte Subsets Temperature Transplantation, Homologous

Connections (1)

This publication is referenced by other Labnodes entities:

Links