The potential role of indoleamine 2,3 dioxygenase (IDO) as a predictive and therapeutic target for diabetes treatment: A mythical truth

Babak Baban, W. Todd Penberthy, Mahmood S Mozaffari

Research output: Contribution to journalReview article

7 Citations (Scopus)

Abstract

Type 1 diabetes (T1D) is an autoimmune disease in which a T-cell-mediated reaction demolishes insulinproducing cells of pancreatic islets. Inadequacy of insulin therapy has motivated research focused on mechanisms by which autoimmune reactions can be suppressed. In recent years, the role of indoleamine 2,3 dioxygenase (IDO) in regulation of immune system has been extensively investigated. Initially, IDOwas recognized as a host defensemechanism. However, recent studies have suggested an immunomodulatory role for IDO which may contribute to the induction of immune tolerance. In this review, we concentrate on the role of IDO in several pathologic conditions with a focus on T1D to rationalize our hypothesis regarding the potential for inclusion of IDO in certain therapeutic strategies aimed at early detection, treatment or ideally cure of chronic and autoimmune diseases such as T1D.

Original languageEnglish (US)
Pages (from-to)46-55
Number of pages10
JournalEPMA Journal
Volume1
Issue number1
DOIs
StatePublished - Jan 1 2010

Fingerprint

Indoleamine-Pyrrole 2,3,-Dioxygenase
Medical problems
Type 1 Diabetes Mellitus
Autoimmune Diseases
Immune Tolerance
T-cells
Immune system
Therapeutics
Islets of Langerhans
Immune System
Chronic Disease
Insulin
T-Lymphocytes
Research

Keywords

  • IDO
  • Individual tolerance
  • Predictive diagnostic
  • Targeted treatment
  • Type 1 diabetes

ASJC Scopus subject areas

  • Drug Discovery
  • Health Policy
  • Biochemistry, medical

Cite this

The potential role of indoleamine 2,3 dioxygenase (IDO) as a predictive and therapeutic target for diabetes treatment : A mythical truth. / Baban, Babak; Penberthy, W. Todd; Mozaffari, Mahmood S.

In: EPMA Journal, Vol. 1, No. 1, 01.01.2010, p. 46-55.

Research output: Contribution to journalReview article

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