Pathophysiology of interleukin-23 in experimental autoimmune encephalomyelitis

Tarik Touil, Denise Fitzgerald, Guang Xian Zhang, A. M. Rostami*, Bruno Gran

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

22 Citations (Scopus)

Abstract

Interleukin-23 (IL-23) is a heterodimeric cytokine that is composed of a p40 subunit, shared with the closely related cytokine IL-12, and a smaller IL-23p19 subunit. It belongs to a family of heterodimeric cytokines that also includes IL-12 and IL-27. Experimental autoimmune encephalomyelitis (EAE) is an autoimmune disease that serves as a model for multiple sclerosis, an inflammatory demyelinating disease of the central nervous system that is a frequent cause of disability in young adults. EAE is thought to be initiated by CD4+ T cells. The production of interferon-gamma and tumor necrosis factor-α (T helper 1 [Th1] phenotype) was considered a marker for the ability of such cells to induce disease. Consistent with this view, IL-12, a cytokine that induces the differentiation of Th1 cells, was considered essential for EAE susceptibility. However, it is now clear that IL-23 rather than IL-12 is required for EAE susceptibility. IL-23 induces a population of IL-17-producing cells that is more critically involved in EAE pathogenesis than Th1 cells. Here, we review the role of the IL-23 system in the pathophysiology of EAE.

Original languageEnglish
Pages (from-to)77-83
Number of pages7
JournalDrug News and Perspectives
Volume19
Issue number2
DOIs
Publication statusPublished - 01 Mar 2006
Externally publishedYes

ASJC Scopus subject areas

  • Pharmacology
  • Drug Discovery

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