| First Author | Liu R | Year | 2008 |
| Journal | Exp Neurol | Volume | 211 |
| Issue | 1 | Pages | 14-24 |
| PubMed ID | 18353312 | Mgi Jnum | J:136857 |
| Mgi Id | MGI:3797203 | Doi | 10.1016/j.expneurol.2007.11.004 |
| Citation | Liu R, et al. (2008) IL-21 receptor expression determines the temporal phases of experimental autoimmune encephalomyelitis. Exp Neurol 211(1):14-24 |
| abstractText | 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. |
