B cells produce pathogenic antibodies and impair recovery after spinal cord injury in mice

The Journal of Clinical Investigation, 2009 · DOI: 10.1172/JCI39780 · Published: October 1, 2009

Simple Explanation

Traumatic spinal cord injury activates B cells, leading to the production of auto-antibodies. This study investigates the functional role of this immune response in mice. Mice lacking B cells showed improved locomotor recovery and reduced lesion pathology after spinal cord injury, indicating B cells impair recovery. Antibodies produced after spinal cord injury contribute to pathology by activating complement and cells with Fc receptors. Targeting this immune response could be a therapeutic strategy.

Study Duration

9 weeks

Participants

Mice with and without B cells

Evidence Level

Not specified

Key Findings

1
Mice lacking B cells showed improved locomotor recovery and reduced lesion volume compared to wild-type mice after spinal cord injury.
2
Antibodies and complement component C1q accumulated at sites of axon pathology and demyelination in mice with normal B cell function after SCI.
3
Injection of antibodies purified from SCI mice into naive mice caused paralysis and neuropathology, demonstrating a direct pathogenic effect of these antibodies.

Research Summary

This study demonstrates that B cells, through antibody production, negatively impact recovery after spinal cord injury (SCI) in mice. Mice lacking B cells exhibit improved locomotor function and reduced lesion pathology. The presence of antibodies and antibody-secreting cells in the cerebrospinal fluid and injured spinal cord of wild-type mice suggests a pathogenic role for B cell-mediated immune responses. Antibodies produced after SCI induce pathology by activating complement and Fc receptors, indicating potential therapeutic targets for SCI treatment.

Practical Implications

Therapeutic Target Identification

Components of the pathologic immune response mediated by B cells and antibodies could be novel targets for minimizing tissue injury and promoting repair after SCI.

B Cell Inhibition

Controlled inhibition of B cells or plasmapheresis (plasma exchange) should be considered as therapeutic options for treating SCI.

Complement Inhibition

Targeting complement activation pathways may provide a therapeutic strategy to reduce antibody-mediated pathology following SCI.

Study Limitations

1
The specific self/auto antigens recognized by SCI-induced antibodies are not fully known.
2
The exact mechanisms by which autoantibodies antagonize endogenous repair mechanisms require further investigation.
3
The study focuses on a murine model, and further research is needed to determine the translatability of these findings to humans.

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