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From the Department of Neurology (Dr. Sharief), United Medical and Dental School, Guy’s Hospital; Departments of Clinical Neurophysiology (Dr. Ingram) and Neurology (Dr. Swash), The Royal London Hospital; and Department of Neuroimmunology (Dr. Thompson), Institute of Neurology, London, England.
Address correspondence and reprint requests to Dr. M.K. Sharief, Department of Neurology, Guy’s Hospital, London SE1 9RT, England.
BACKGROUND: Treatment with human IV immunoglobulin (IVIg) modifies the course of Guillain-Barré syndrome (GBS), but its specific mode of action is unknown. Cellular interactions mediated through the release of cytokines play a role in the pathogenesis of GBS and may be regulated by IVIg therapy.
OBJECTIVE: To delineate possible immunoregulatory mechanisms of IVIg in patients with GBS.
METHODS: Circulating levels of the proinflammatory cytokines, tumor necrosis factor (TNF)-
and interleukin (IL)-1ß, were assayed in 21 patients with GBS before and serially after IVIg therapy. Comparisons were made with serum concentration of the anti-inflammatory cytokines, soluble TNF- receptor and IL-10. Serial measurements were also performed in 12 untreated patients with relatively mild disease and 7 patients treated by plasma exchange.
RESULTS: Circulating levels of TNF- and IL-1ß decreased after treatment with IVIg but remained relatively high in untreated patients and in those treated by plasma exchange. Clinical improvement in patients treated with IVIg was associated with a reduction in unbound TNF- during the acute phase of the illness. Circulating levels of anti-inflammatory cytokines were not affected by IVIg treatment.
CONCLUSION: Data presented here suggest a novel mechanism of action of IVIg that involves selective modulation of circulating proinflammatory cytokines.
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