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Monitoring Immune Cells Trafficking Fluorescent Prion Rods Hours after Intraperitoneal Infection
Published on: November 19, 2010
Alteration of B-cell subsets enhances neuroinvasion in mouse scrapie infection
Christine von Poser-Klein1, Eckhard Flechsig, Tanja Hoffmann
1Institute of Virology and Immunobiology, University of Würzburg, Versbacherstr. 7, D-97078 Würzburg, Germany.
Abstract:
Acquired forms of prion diseases or transmissible spongiform encephalopathies are believed to occur following peripheral exposure. Prions initially accumulate in the lymphoid system before spreading to the nervous system, but the underlying mechanisms for prion transfer between the two systems are still elusive. Here we show that ablation of the B-cell-specific transmembrane protein CD19, a coreceptor of the complement system, results in an acceleration of prion neuroinvasion. This appears to be due to an alteration of the follicular dendritic cell (FDC) network within the lymphoid tissue, thereby reducing the distance between FDCs and adjacent nerve fibers that mediate prion neuroinvasion.
Insights
Removing CD19, a B-cell protein, accelerates prion neuroinvasion by altering the follicular dendritic cell network. This brings prions closer to nerves, speeding up spread to the nervous system.
Area of Science:
- Neuroscience
- Immunology
- Prion Biology
Background:
- Acquired prion diseases (transmissible spongiform encephalopathies) originate from peripheral exposure.
- Prions first accumulate in lymphoid tissues before affecting the nervous system.
- Mechanisms of prion transfer from lymphoid to nervous systems remain unclear.
Purpose of the Study:
- To investigate the role of CD19 in prion neuroinvasion.
- To elucidate the mechanisms of prion spread from lymphoid tissues to the nervous system.
Main Methods:
- Ablation of the B-cell-specific transmembrane protein CD19 in a model system.
- Analysis of prion accumulation and spread within lymphoid and nervous tissues.
- Examination of the follicular dendritic cell (FDC) network structure and proximity to nerve fibers.
Main Results:
- Ablation of CD19 accelerated prion neuroinvasion.
- CD19 deficiency altered the follicular dendritic cell (FDC) network.
- The altered FDC network reduced the distance between FDCs and nerve fibers, facilitating prion transfer.
Conclusions:
- CD19 plays a crucial role in regulating the FDC network structure within lymphoid tissues.
- The FDC network's organization is critical for controlling the rate of prion neuroinvasion.
- Targeting CD19 or the FDC network could offer strategies to prevent prion disease spread.
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