Molecular pathways altered by insulin B9-23 immunization

Sarah E. Eckenrode, Qing Guo Ruan, Christin D. Collins, Ping Yang, Richard A McIndoe, Andrew Muir, Jin-Xiong She

Research output: Contribution to journalArticle

4 Scopus citations

Abstract

Type 1 diabetes (T1D) in the nonobese diabetic (NOD) mouse can be delayed by administration of insulin or specific insulin peptides. To better understand how insulin treatment delays diabetes development, NOD mice treated with an insulin peptide (B9-23) were compared with age-matched NOD and NOD congenic mice for gene expression changes in spleen using cDNA microarray. Fifty genes were identified that were significantly altered by B9-23 treatment. Thirty-three of these genes are downregulated by the treatment while they are upregulated during the natural disease progression in NOD from immature (3-4 weeks) to mature (10 weeks) stages. Taken together, our data suggest that the B9-23 treatment, like the protective genes in NOD congenic strains, reduces pro-inflammatory activation of lymphocytes that normally occurs in NOD mice. Furthermore, our studies discovered two genes (Irf4 and Tra1) with increased expression in B9-23-treated mice that promote the Th2 response, providing a molecular basis for the B9-23-protective therapy.

Original languageEnglish (US)
Pages (from-to)175-185
Number of pages11
JournalAnnals of the New York Academy of Sciences
Volume1037
DOIs
StatePublished - Jan 1 2004

Keywords

  • B9-23 treatment
  • Insulin
  • Microarray
  • NOD
  • Th1/Th2 balance

ASJC Scopus subject areas

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • History and Philosophy of Science

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