| First Author | Zabel MD | Year | 2007 |
| Journal | J Immunol | Volume | 179 |
| Issue | 9 | Pages | 6144-52 |
| PubMed ID | 17947689 | Mgi Jnum | J:152995 |
| Mgi Id | MGI:4360583 | Doi | 10.4049/jimmunol.179.9.6144 |
| Citation | Zabel MD, et al. (2007) Stromal complement receptor CD21/35 facilitates lymphoid prion colonization and pathogenesis. J Immunol 179(9):6144-52 |
| abstractText | We have studied the role of CD21/35, which bind derivatives of complement factors C3 and C4, in extraneural prion replication and neuroinvasion. Upon administration of small prion inocula, CD21/35(-/-) mice experienced lower attack rates and delayed disease over both wild-type (WT) mice and mice with combined C3 and C4 deficiencies. Early after inoculation, CD21/35(-/-) spleens were devoid of infectivity. Reciprocal adoptive bone marrow transfers between WT and CD21/35(-/-) mice revealed that protection from prion infection resulted from ablation of stromal, but not hemopoietic, CD21/35. Further adoptive transfer experiments between WT mice and mice devoid of both the cellular prion protein PrP(C) and CD21/35 showed that splenic retention of inoculum depended on stromal CD21/35 expression. Because both PrP(C) and CD21/35 are highly expressed on follicular dendritic cells, CD21/35 appears to be involved in targeting prions to follicular dendritic cells and expediting neuroinvasion following peripheral exposure to prions. |
