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In This Issue, The Journal of Immunology, Volume 179, Issue 9, November 2007, Pages 5615–5616, https://doi.org/10.4049/jimmunol.179.9.5615
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Prions and Complement
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Complement activation is known to be involved in the pathogenesis of prion diseases. As prion accumulation in lymphoid tissues often precedes neuroinvasion in these diseases, Zabel et al. (p. 6144 ) analyzed the role of CD21/35 complement receptors in early disease pathogenesis. Ablation of CD21/35 significantly delayed prion disease, and this delay was significantly longer than that observed in mice lacking the ligands for CD21/35, C3 and C4. Delayed disease progression in CD21/35−/− mice was accompanied by decreased prion accumulation in the spleen, suggesting that CD21/35 might enhance splenic prion protein retention. Indeed, experiments using reciprocal bone marrow chimeras (CD21/35−/−→wild type or wild type→CD21/35−/−) demonstrated a requirement for CD21/35 expression on stromally derived cells, presumably follicular dendritic cells (FDCs), for prion accumulation and retention. Interestingly, bone marrow chimeras lacking CD21/35 on B cells also demonstrated a delay in disease progression, indicating that FDCs are not the only CD21/35+ cells required for efficient prion disease pathogenesis. However, the data implicated CD21/35 on FDCs as important in targeting prions to FDCs and in subsequent disease development.
