John Dawes

Associate Professor

Principal Investigator
Course Director, MSc Pain Neurosciences

Research Summary

It is now well established that the immune system contributes to pathological pain sates and one relatively under studied aspect of this is through the action of autoantibodies. Neuropathic pain is common in patients with autoantibodies directed against components of the voltage gated potassium channel complex such as CASPR2 and LGI1. By using patient samples in combination with basic pain research my aim is to better understand the mechanisms of autoantibody mediated pain and by doing so uncover novel molecular pathways regulating pain sensitivity as well as revealing clinically relevant targets for the development of future therapies.

Immune or Genetic-Mediated Disruption of CASPR2 Causes Pain Hypersensitivity Due to Enhanced Primary Afferent Excitability

Dawes JM. et al, (2018), Neuron, 97, 806 - 822.e10

Autoantibodies and neuropathic pain

Dawes JM. and Bennett DL., (2018), 833 - 850

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Contact information

Funding

Research groups

Colleges

Collaborators

David Bennett

Sarosh Irani

John Dawes

Research Summary

Key publications

Autoantibodies as drivers of neuropathic pain.

A role for leucine-rich, glioma inactivated 1 in regulating pain sensitivity

A role for pathogenic autoantibodies in small fiber neuropathy?

Immune or Genetic-Mediated Disruption of CASPR2 Causes Pain Hypersensitivity Due to Enhanced Primary Afferent Excitability

Autoantibodies and neuropathic pain

Recent publications

Recent advances in autoantibody-mediated pain

Autoantibodies as drivers of neuropathic pain.

Understanding sensory abnormalities in fibromyalgia through autoantibodies

Specific overexpression of contactin-associated protein-like 2 and its effects on pain-related behaviour in mice

A role for leucine-rich, glioma inactivated 1 in regulating pain sensitivity