Transient increase in symptoms associated with cytokine release in patients with multiple sclerosis (original) (raw)

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University of Cambridge Neurology unit, Addenbrooke's Hospital

Oxford, UK

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University of Cambridge Neurology unit, Addenbrooke's Hospital

Oxford, UK

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Molecular Immunopathology Unit, MRC Centre

Oxford, UK

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Division of Immunology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital

Oxford, UK

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Division of Immunology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital

Oxford, UK

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Sir William Dunn School of Pathology

Oxford, UK

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Division of Immunology, Department of Pathology, University of Cambridge, Addenbrooke's Hospital

Oxford, UK

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Sir William Dunn School of Pathology

Oxford, UK

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University of Cambridge Neurology unit, Addenbrooke's Hospital

Oxford, UK

4

MRC Cambridge Centre for Brain Repair

Cambridge, Oxford, UK

Professor Alastair Compston, University of Cambridge Neurology unit, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK

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Revision received:

17 July 1995

Published:

01 February 1996

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Thibault Moreau, Alasdair Coles, Mark Wing, John Isaacs, Geoffrey Hale, Herman Waldmann, Alastair Compston, Transient increase in symptoms associated with cytokine release in patients with multiple sclerosis, Brain, Volume 119, Issue 1, February 1996, Pages 225–237, https://doi.org/10.1093/brain/119.1.225
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Abstract

Summary

Fourteen patients with multiple sclerosis were treated with the humanized monoclonal antibody CAMPATH-IH which targets the CD52 antigen present on all lymphocytes and some monocytes; four also received anti-CD4 antibody. Lymphopaenia developed rapidly and was sustained for at least 1 year. In 12 patients, the first infusion of antibody was characterized by significant exacerbation or re-awakening of pre-existing symptoms lasting several hours. These clinical effects of antibody treatment correlated with increased levels of circulating cytokines. Peak levels of tumour necrosis factor (TNF)-α and interferon (IFN)-γ occurred at 2 h, whereas the rise in interleukin-6 (IL-6) was significantly delayed and peaked at 4 h after starting antibody treatment. There was a decline in CH50, indicating complement activation. The neurological symptoms could not be attributed directly to pyrexia and were not provoked (in one patient) by an artificial rise in temperature. In the remaining two patients, a single pre-treatment with intravenous methylprednisolone (500 mg) prevented both the transient increase in neurological symptoms and the cytokine release. Our results, involving 14 intensively studied patients treated with humanized monoclonal antibodies, suggest that soluble immune mediators contribute to symptom production in multiple sclerosis; the mechanism remains uncertain but, on the available evidence, we favour the interpretation that cytokines directly affect conduction through partially demyelinated pathways.

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Topic:

• cytokine
• tumor necrosis factors
• biological response modifiers
• fever
• monoclonal antibodies
• complement activation
• complement hemolytic activity assay
• interferons
• lymphocytes
• methylprednisolone
• monocytes
• multiple sclerosis
• neurologic manifestations
• antibodies
• body temperature
• interleukin-6
• temperature
• immune mediator
• human leukocyte interferon
• awakening
• cd52 antigen
• infusion procedures

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