| First Author | Barbour M | Year | 2014 |
| Journal | Eur J Immunol | Volume | 44 |
| Issue | 11 | Pages | 3320-9 |
| PubMed ID | 25116404 | Mgi Jnum | J:250084 |
| Mgi Id | MGI:6101834 | Doi | 10.1002/eji.201444671 |
| Citation | Barbour M, et al. (2014) IL-33 attenuates the development of experimental autoimmune uveitis. Eur J Immunol 44(11):3320-9 |
| abstractText | Interleukin-33 (IL-33) is associated with several important immune-mediated disorders. However, its role in uveitis, an important eye inflammatory disease, is unknown. Here, we investigated the function of IL-33 in the development of experimental autoimmune uveitis (EAU). IL-33 and IL-33 receptor (ST2) were expressed in murine retinal pigment epithelial (RPE) cells in culture, and IL-33 increased the expression of Il33 and Mcp1 mRNA in RPE cells. In situ, IL-33 was highly expressed in the inner nuclear cells of the retina of naive mice, and its expression was elevated in EAU mice. ST2-deficient mice developed exacerbated EAU compared with WT mice, and administration of IL-33 to WT mice significantly reduced EAU severity. The attenuated EAU in IL-33-treated mice was accompanied by decreased frequency of IFN-gamma+ and IL-17(+) CD4+ T cells and reduced IFN-gamma and IL-17 production but with increased frequency of IL-5(+) and IL-4(+) CD4 T cells and IL-5 production in the draining lymph node and spleen. Macrophages from the IL-33-treated mice show a significantly higher polarization toward an alternatively activated macrophage phenotype. Our results therefore demonstrate that the endogenous IL-33/ST2 pathway plays an important role in EAU, and suggest that IL-33 represents a potential option for treatment of uveitis. |
