Journal
JOURNAL OF IMMUNOLOGY
Volume 188, Issue 5, Pages 2118-2126Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1103342
Keywords
-
Categories
Funding
- Juvenile Diabetes Research Foundation [1-2005-039, 5-2006-918, 5-2006-403]
- American Diabetes Association [7-05-JF-30]
- Henry Ford Immunology Program start-up [T71016, T71017]
Ask authors/readers for more resources
CD1d-restricted V alpha 14 invariant NKT (iNKT) cells play an important role in the regulation of diverse immune responses. MicroRNA-mediated RNA interference is emerging as a crucial regulatory mechanism in the control of iNKT cell differentiation and function. Yet, roles of specific microRNAs in the development and function of iNKT cells remain to be further addressed. In this study, we identified the gradually increased expression of microRNA-150 (miR-150) during the maturation of iNKT cells in thymus. Using miR-150 knockout (KO) mice, we found that miR-150 deletion resulted in an interruption of iNKT cell final maturation in both thymus and periphery. Upon activation, iNKT cells from miR-150KO mice showed significantly increased IFN-gamma production compared with wild-type iNKT cells. Bone marrow-transferring experiments demonstrated the cell-intrinsic characteristics of iNKT cell maturation and functional defects in mice lacking miR-150. Furthermore, miR-150 target c-Myb was significantly upregulated in miR-150KO iNKT cells, which potentially contribute to iNKT cell defects in miR-150KO mice. Our data define a specific role of miR-150 in the development and function of iNKT cells. The Journal of Immunology, 2012, 188: 2118-2126.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available