September 2026

RHEUMATOLOGY

COULD NEUROIMMUNE MODULATION OFFER A NEW APPROACH TO RA? Q&A WITH ERIC RUDERMAN, MD

Key Takeaways
  • Vagus nerve stimulation (VNS) targets neuroimmune signaling rather than a single cytokine or receptor.
  • The larger significance is the possibility that neural pathways could become another therapeutic avenue in rheumatology.
  • The downstream mechanisms are not fully defined, so the concept should be interpreted with appropriate caution.
 
Why are rheumatologists interested in VNS?
We've known for years that the nervous system and immune system communicate with one another. Research has explored the role of the vagus nerve in maintaining immunologic balance and regulating inflammatory cytokine production. The question is whether we can intentionally use those pathways to treat inflammatory diseases.
 
How might VNS reduce inflammation?
The full mechanism is not completely defined. Research suggests that signaling between the vagus nerve and spleen may increase acetylcholine signaling and influence inflammatory cytokine production, including TNF.

There is also evidence of potential effects on pathways such as JAK-STAT signaling and gene transcription. It is important not to oversimplify the biology. This is not as straightforward as blocking a single cytokine or receptor, and we are still learning which downstream effects matter clinically.
 
How is this different from current RA therapies?
Most of our therapies target a specific inflammatory pathway. TNF inhibitors block TNF activity, while JAK inhibitors interfere with intracellular signaling. VNS is different because it uses neural signaling to modulate inflammation and may affect multiple downstream pathways.
 
Why does this matter beyond the device itself?
What makes this interesting isn't simply the device. The clinical evidence suggests that targeting neural pathways can affect disease activity in RA. If that concept continues to hold up, neuroimmune modulation could open another therapeutic avenue for inflammatory disease.
Eric M. Ruderman, MD, Professor of Rheumatology at Northwestern Medicine​

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