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Updated: Nov 26, 2025

Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination
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CNS demyelination during tofacitinib therapy: First report

Fathi Massoud1, Ismail Ibrahim Ismail1, Jasem Y Al-Hashel2

  • 1Department of Neurology, Ibn Sina Hospital, Kuwait.

Multiple Sclerosis and Related Disorders
|December 10, 2020
PubMed

Insights

Tofacitinib, a Janus kinase inhibitor, may cause reversible central nervous system demyelination in rheumatoid arthritis patients. This rare side effect might involve T17 cell activation and interleukin-17 production.

Area of Science:

  • Neurology
  • Immunology
  • Rheumatology

Background:

  • Iatrogenic demyelination is a rare central nervous system (CNS) inflammatory disorder.
  • Tofacitinib, a Janus kinase (JAK) inhibitor, is used for rheumatoid arthritis but has shown mixed results in multiple sclerosis animal models.

Discussion:

  • This report details a unique case of reversible multifocal CNS demyelination in a patient with seropositive rheumatoid arthritis treated with tofacitinib.
  • The proposed mechanism involves tofacitinib-induced activation of T17 cells, leading to increased interleukin-17 (IL-17) production.
  • A potential link between tumor necrosis factor-alpha (TNF-α) and JAK/STAT pathways may also contribute to this iatrogenic demyelination.

Key Insights:

  • Novel case of drug-induced demyelination linked to JAK inhibitor therapy.
  • Potential role of T17 cell activation and IL-17 in tofacitinib-associated CNS inflammation.
  • Highlights the complexity of JAK inhibitor effects in autoimmune diseases.

Outlook:

  • Further research is needed to elucidate the precise mechanisms of tofacitinib-induced demyelination.
  • Monitoring for neurological adverse events in patients on JAK inhibitors is crucial.
  • This case may inform risk-benefit assessments for tofacitinib in autoimmune conditions.
Keywords:
DemyelinationIatrogenicJanus kinase inhibitorMultiple sclerosisTofacitinib

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