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The role of complement in spongiform encephalopathies

Depletion of complement factors or the complement receptor significantly delays the onset of scrapies in a mouse model.

Tudor Toma(ttoma@mail.dntis.ro)

Agents of transmissible spongiform encephalopathies (TSEs) usually enter the body via a peripheral route and replicate in lymphoreticular tissues before moving into the brain. Any impairment of the lymphoreticular system slows transfer of the TSE agent to the brain and delays the clinical onset of symptoms. In the April Nature Medicine, Klein et al and Mabbott et al show that complement factors are involved in the uptake of TSE-inducing agents by the lymphoreticular system and that their absence can delay CNS invasion.

In the two independent studies on mouse models of scrapie Klein et al from The University of Zurich, and Mabbott et al from Institute for Animal Health in Edinburgh, showed that depletion of either one of the early complement factors (C1q, Bf/C2 and C3) or the complement receptor (CR1/2) significantly delays the onset of disease symptoms in mice injected with limiting doses of the scrapie strains...

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