| First Author | Tsukuba T | Year | 2003 |
| Journal | J Biochem | Volume | 134 |
| Issue | 6 | Pages | 893-902 |
| PubMed ID | 14769879 | Mgi Jnum | J:108745 |
| Mgi Id | MGI:3624616 | Doi | 10.1093/jb/mvg216 |
| Citation | Tsukuba T, et al. (2003) Association of cathepsin E deficiency with development of atopic dermatitis. J Biochem 134(6):893-902 |
| abstractText | Atopic dermatitis (AD) is a pruritic inflammatory skin diseases associated with a family history of atropy. Here we show that mice lacking the endolysosomal aspartic proteinase cathepsin E spontaneously develop skin lesions similar to those of humans with AD when reared under conventional conditions but not under specific pathogen-free conditions. These mice showed the increase in the ratio of CD4+/CD8+ T cells, the strong polarization of naive T cells to T helper 2 cells, and the systemic accumulation of IL-18 and IL-1beta accompanied by a marked increase in IL-4, IL-5, and IgE. The relative rates of degradation of IL-18 and IL-1beta were significantly lower in cathepsin E-deficient mice than wild-type mice. These results strongly suggest that the development of AD in cathepsin E-deficient mice is initiated by systemic accumulation of IL-18 and IL-1beta, mainly due to their reduced turnover rates. In addition, the reduced expression of cathepsin E was also observed in erythrocytes of both humans with AD and the AD mouse model NC/Nga. Cathepsin E deficiency might thus be responsible for the induction of AD in humans and mice. |
