کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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3056653 | 1186573 | 2008 | 11 صفحه PDF | دانلود رایگان |

The IL-21 receptor (IL-21R) consists of a unique subunit and a common γ chain (γc) 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.
Journal: Experimental Neurology - Volume 211, Issue 1, May 2008, Pages 14–24