Immune modulation for prevention of type 1 diabetes mellitus

  • Itamar Raz
  • , Roy Eldor*
  • , Yaakov Naparstek
  • *Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

47 Scopus citations

Abstract

Prevention of type 1 diabetes mellitus requires early intervention in the autoimmune process directed against β cells of the pancreatic islets of Langerhans. This autoimmune inflammatory process is thought to be caused by the effect of Th1 cells and their secreted cytokines (e.g. interferon) and to be suppressed by Th2-secreted anti-inflammatory cytokines (e.g. IL-4, IL-10). Various methods aimed specifically at halting or modulating this response have been attempted. An alternative method is the re-induction of tolerance towards the putative self antigen that causes the disease. Proposed antigens such as insulin, glutamic acid decarboxilase (GAD) and the heat shock protein 60 (Hsp60)-derived peptide 277 have been used successfully in murine diabetes models and in initial clinical trials in early diabetes patients. Here, we review the results of these trials.

Original languageEnglish
Pages (from-to)128-134
Number of pages7
JournalTrends in Biotechnology
Volume23
Issue number3
DOIs
StatePublished - Mar 2005
Externally publishedYes

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