Permanent URL to this publication: http://dx.doi.org/10.5167/uzh-60877
Zabel, M D; Heikenwalder, M; Prinz, M; Arrighi, I; Schwarz, P; Kranich, J; von Teichman, A; Haas, K M; Zeller, N; Tedder, T F; Weis, J H; Aguzzi, A (2007). Stromal complement receptor CD21/35 facilitates lymphoid prion colonization and pathogenesis. Journal of Immunology, 179(9):6144-6152.
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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.
|Item Type:||Journal Article, refereed, original work|
|Communities & Collections:||04 Faculty of Medicine > University Hospital Zurich > Institute of Neuropathology|
|DDC:||570 Life sciences; biology|
610 Medicine & health
|Deposited On:||04 Jul 2012 16:28|
|Last Modified:||27 Nov 2013 18:37|
|Publisher:||American Association of Immunologists|
|Free access at:||PubMed ID. An embargo period may apply.|
|Citations:||Web of Science®. Times cited: 31|
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