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Related Experiment Video

Updated: Jul 10, 2026

Isolation of Murine Lymph Node Stromal Cells

Isolation of Murine Lymph Node Stromal Cells

Published on: August 19, 2014

Stromal complement receptor CD21/35 facilitates lymphoid prion colonization and pathogenesis.

Mark D Zabel¹, Mathias Heikenwalder, Marco Prinz

¹Institute for Neuropathology, University Hospital of Zürich, Zürich, Switzerland. mark.zabel@colostate.edu

Journal of Immunology (Baltimore, Md. : 1950)

|October 20, 2007

Summary

The complement receptor CD21/35 on stromal cells is crucial for prion replication and neuroinvasion. Ablating this receptor significantly delays prion disease by preventing splenic prion retention.

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Area of Science:

Immunology
Neuroscience
Infectious Diseases

Background:

Prion diseases are fatal neurodegenerative disorders.
Extraneural prion replication and neuroinvasion are key to disease pathogenesis.
Complement receptors CD21/35 bind complement factors C3 and C4, implicated in immune responses.

Purpose of the Study:

To investigate the role of CD21/35 in extraneural prion replication and neuroinvasion.
To determine the cellular source of CD21/35 mediating prion susceptibility.

Main Methods:

Utilized CD21/35 knockout (CD21/35(-/-)) mice and wild-type (WT) mice.
Administered small prion inocula to assess disease progression and attack rates.
Performed reciprocal adoptive bone marrow transfers to distinguish stromal vs. hemopoietic roles.
Conducted further transfers with mice lacking both cellular prion protein (PrP(C)) and CD21/35.

Main Results:

CD21/35(-/-) mice showed reduced attack rates and delayed prion disease onset compared to WT mice.
Early splenic infectivity was absent in CD21/35(-/-) mice post-inoculation.
Protection against prion infection was attributed to the absence of stromal CD21/35, not hemopoietic.
Stromal CD21/35 expression was essential for splenic retention of prion inocula.

Conclusions:

CD21/35 on follicular dendritic cells plays a critical role in prion targeting and neuroinvasion.
Stromal CD21/35 mediates the initial splenic retention of prions following peripheral exposure.
Targeting CD21/35 may offer a therapeutic strategy to prevent prion neuroinvasion.