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Exp Neurol. 2008 May;211(1):14-24. doi: 10.1016/j.expneurol.2007.11.004. Epub 2007 Nov 22.

IL-21 receptor expression determines the temporal phases of experimental autoimmune encephalomyelitis.

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  • 1Department of Neurology, Barrow Neurological Institute, St. Joseph's Hospital and Medical Center, 350 West Thomas Road, Phoenix, AZ 85013, USA.

Abstract

The IL-21 receptor (IL-21R) consists of a unique subunit and a common gamma chain (gamma(c)) that is shared with other cytokines including IL-2, IL-4, IL-7, and IL-15. The interaction between IL-21 and IL-21R results in significant effects on both innate and adaptive immune responses. In this study we examined the influence of IL-21R deficiency (IL-21R(-/-)) on the development of experimental autoimmune encephalomyelitis (EAE), an animal model of human multiple sclerosis (MS). IL-21R(-/-) mice developed EAE earlier and more severe neurological impairment than control mice, yet those mice could effectively recover from neurological deficits. The impact on EAE initiation by IL-21R deficiency was associated with a defect of CD4(+)CD25(+) T regulatory (Treg) cells and a down-regulated expression of Foxp3. The recovery from IL-21R(-/-) EAE was correlated with an expansion of Treg cells as well as an organ-specific redistribution of NK cells. These results suggest that a temporal influence of IL-21 on the activity of immunoregulatory circuits can be important in the modulation of the course of the autoimmune disease.

PMID:
18353312
DOI:
10.1016/j.expneurol.2007.11.004
[PubMed - indexed for MEDLINE]
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