IV immunoglobulin reduces circulating proinflammatory cytokines in Guillain-Barré syndrome

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Abstract
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)-α and interleukin (IL)-1β, 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-α 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-α and IL-1β 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-α 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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