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Related Experiment Videos

Complement facilitates early prion pathogenesis.

M A Klein1, P S Kaeser, P Schwarz

  • 1Institute of Neuropathology, University of Zurich, Schmelzbergstrasse, Zurich, Switzerland.

Nature Medicine
|April 3, 2001
PubMed
Summary
This summary is machine-generated.

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The complement system, not antibodies, is crucial for early prion spread in mice. Complement activation aids in trapping prions in lymphoreticular organs after extracerebral exposure.

Area of Science:

  • Neuroimmunology
  • Prion Biology
  • Infectious Diseases

Background:

  • New-variant Creutzfeldt-Jakob disease and scrapie originate from extracerebral exposure, with initial prion replication in lymphoid organs.
  • Follicular dendritic cells (FDCs) are key prion reservoirs, and their maturation, dependent on lymphotoxin and B-lymphocytes, is vital for scrapie pathogenesis.
  • FDCs utilize Fc-gamma receptors for immune complexes and complement receptors (CRs) for C3d/C4b-opsonized antigens.

Purpose of the Study:

  • To investigate the role of Fc-gamma receptors and complement system components in peripheral prion pathogenesis.
  • To determine the mechanisms involved in the initial trapping of prions in lymphoreticular organs following extracerebral exposure.

Main Methods:

  • Mice were subjected to B-lymphocyte depletion, immunoglobulin depletion, or deficiency in Fc-gamma receptors.

Related Experiment Videos

  • Complement-deficient mice (lacking C3, C1q, Bf/C2, or CRs) were used to assess protection against scrapie.
  • Mice were inoculated intraperitoneally with limiting amounts of prions, and prion infectivity and PrPSc accumulation in the spleen were monitored.

    • Main Results:

    • Depletion of immunoglobulins or Fc-gamma receptors did not affect scrapie pathogenesis if B-cell maturation remained intact.
    • Mice deficient in complement components (C3, C1q, Bf/C2) or complement receptors showed partial or full protection against prion disease.
    • Splenic accumulation of prion infectivity and PrPSc was delayed in complement-deficient mice, indicating impaired initial prion trapping.

    Conclusions:

    • Complement activation, rather than antibody-mediated mechanisms via Fc-gamma receptors, is critical for the initial phase of peripheral prion pathogenesis.
    • Specific complement components play a significant role in the early trapping of prions within lymphoreticular organs after extracerebral exposure.
    • Targeting complement activation pathways may offer a therapeutic strategy to prevent prion neuroinvasion.