Pathophysiology of interleukin-23 in experimental autoimmune encephalomyelitis.
Publication/Presentation Date
3-1-2006
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-alpha (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.
Volume
19
Issue
2
First Page
77
Last Page
83
ISSN
0214-0934
Published In/Presented At
Touil, T., Fitzgerald, D., Zhang, G. X., Rostami, A. M., & Gran, B. (2006). Pathophysiology of interleukin-23 in experimental autoimmune encephalomyelitis. Drug news & perspectives, 19(2), 77–83. https://doi.org/10.1358/dnp.2006.19.2.977443
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
16628262
Department(s)
Administration and Leadership
Document Type
Article