| First Author | Teruya K | Year | 2022 |
| Journal | Int Immunopharmacol | Volume | 107 |
| Pages | 108672 | PubMed ID | 35279511 |
| Mgi Jnum | J:325675 | Mgi Id | MGI:7281267 |
| Doi | 10.1016/j.intimp.2022.108672 | Citation | Teruya K, et al. (2022) Anti-prion activity of cellulose ether is impaired in mice lacking pre T-cell antigen receptor alpha, T-cell receptor delta, or lytic granule function. Int Immunopharmacol 107:108672 |
| abstractText | The anti-prion activity of cellulose ether (CE) has been reported in rodents, but the mechanism of action is not well understood. As defects in early T-cell development have been reported in Tga20 mice which show only a slight effect of CE administration, we investigated the involvement of immune functions in the CE action. We confirmed an insertion of the prion protein transgene into the pre T-cell antigen receptor alpha gene of Tga20 mice, and its impaired expression in the thymus and other tissues. The influence of immune suppression on the CE effect was then examined in high CE-responder mice treated with immunosuppressive agents or neonatal thymectomy. As neonatal thymectomy significantly reduced the CE effect, we compared the influence of various T-cell defects in mice with similar genetic backgrounds. The CE effect was increased or unchanged in mice with defects in the alphabeta T-cell lineage, whereas it was abolished in T-cell receptor delta deficient mice. Further, when other immune defects were examined, the CE effect was reduced in mice with lysosomal trafficking dysfunction, but was unchanged in mice deficient in B-cell differentiation or toll-like receptor 4 signaling. These findings collectively suggest that the mechanism of CE action may involve gammadelta T cells and lytic granule function, as well as immune factors like natural killer T cells which are lacking in pre T-cell antigen receptor alpha deficient mice and neonatally thymectomized mice. |
