Temporary depletion of complement component C3 or genetic deficiency of C1q significantly delays onset of scrapie

Article Abstract:

Research presented concerns the infective ability of transmissible spongiform encephalopathies (TSEs), focusing on TSE replication, prion proteins, and follicular dentritic cells. Findings sugest that a temporary depletion of complement component C3 or genetic deficiency of C1q retards the onset of scrapie and lessens the early accumulation of prion proteins in the body.

Cellular control mechanisms, Cell regulation, Spongiform encephalopathy, Scrapie

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Natural antibodies and complement are endogenous adjuvants for vaccine-induced CD8(sup)+ T-cell responses

Article Abstract:

Research shows that the recognition of pathogen-derived molecules by antibodies and induction of interleukin-4-mediated pathway of CD8+ T-cell priming are linked, suggesting that immune complex-mediated complement activation regulates T-cell-mediated immunity.

Biological Product (except Diagnostic) Manufacturing, Biological products exc. diagnostic, Interleukin, Physiological aspects, Immunity, Immunity (Physiology), Interleukins, T cells, Viral antibodies, Antibodies, CD8 lymphocytes

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Prion disease: bridging the spleen-nerve gap

Article Abstract:

Relevance of lymphoid tissue in transmissible spongiform encephalopathies (TSEs) disease is analyzed. The mechanism of Creutzfeldt-Jakob Disease (CJD) infection and probable prevention of other TSE diseases is depicted.

Science & research, Lymphoid tissue

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