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Updated: Jul 9, 2026

Transfer of Manipulated Tumor-associated Neutrophils into Tumor-Bearing Mice to Study their Angiogenic Potential In Vivo
Published on: July 20, 2019
Tumor necrosis factor-alpha antagonists and neuropathy
1Department of Neurology and Neuroscience, Cornell University Medical College, New York Presbyterian Hospital, 525 East 68th Street, New York, NY 10065-4897, USA. pstuebge@med.cornell.edu
Tumor necrosis factor (TNF)-alpha antagonists can trigger autoimmune neuropathies. Stopping these drugs often resolves nerve damage, suggesting a potential treatment role for TNF-alpha antagonists in specific immune-mediated neuropathies.
Area of Science:
- Neuroimmunology
- Autoimmune Diseases
Background:
- Tumor necrosis factor (TNF)-alpha is crucial for immune regulation and T-cell responses.
- TNF-alpha contributes to the pathogenesis of immune-mediated demyelinating neuropathies.
Purpose of the Study:
- To review the evidence linking TNF-alpha antagonists to autoimmune neuropathies.
- To discuss proposed mechanisms and treatment outcomes.
Main Methods:
- Review of case histories and series.
- Analysis of the association between anti-TNF-alpha therapy and peripheral nerve disorders.
Main Results:
- TNF-alpha antagonists are associated with various peripheral neuropathies, including Guillain-Barré syndrome and CIDP.
- Proposed mechanisms involve T-cell/humoral attack on myelin, vasculitis, and axonal support inhibition.
- Most neuropathies improve upon drug withdrawal, with or without immunotherapy.
Conclusions:
- TNF-alpha antagonists can induce autoimmune neuropathies.
- Withdrawal of TNF-alpha antagonists is an effective treatment.
- Further research is needed on using TNF-alpha antagonists for immune-mediated neuropathies unresponsive to standard therapies.
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