| First Author | Kim S | Year | 2016 |
| Journal | Immunobiology | Volume | 221 |
| Issue | 8 | Pages | 871-8 |
| PubMed ID | 27021907 | Mgi Jnum | J:315437 |
| Mgi Id | MGI:6830421 | Doi | 10.1016/j.imbio.2016.03.008 |
| Citation | Kim S, et al. (2016) Impaired spleen structure and chemokine expression in ME7 scrapie-infected mice. Immunobiology 221(8):871-8 |
| abstractText | We have previously demonstrated that prion protein-deficient (Prnp(0/0)) Zurich I mice display impaired T zone structure resulting from decreased splenic expression of the T cell homing chemokines, CCL19 and CCL21. Prions are transported to, and colonise in, the secondary lymphoid tissues. Therefore, in order to investigate how scrapie infection affects the splenic white pulp structure, we infected C57BL/6 mice with the mouse-adapted scrapie strain ME7 and analysed end-stage prion disease. We found that the white pulp regions of ME7-infected spleens were smaller, and contained markedly diminished T zones, as compared to control spleens. Although lymphoid tissue inducer cells were not affected, the expression of both CCL19 and CCL21 was decreased. In addition, the networks of follicular dendritic cells, which are known to express high levels of the cellular prion protein (PrP(C)) and to accumulate PrP(Sc) following scrapie infection, were larger in ME7-infected spleens. Further, they were associated with increased numbers of B cells expressing high levels of IgM. These data indicate that ME7-infected spleens display phenotype characteristics different from those reported for Prnp(0/0) spleens mainly due to the gain of PrP(Sc) function and suggest that the PrP(C) is required, not only to form the splenic white pulp structure, but also to maintain the intact T zone structure. |
