Tumour necrosis factor-α and other cytokines in Guillain-Barré syndrome

Abstract

The efficacy of plasma exchange implicates myelinotoxic humoral factors in the pathogenesis of Guillain-Barre syndrome. Candidate factors include autoantibodies to peripheral nerve myelin, which are not unique to Guillain-Barré syndrome; and cytokines such as tumour necrosis factor-a (TNF-α) which are T ceWVmacrophage products. Plasma cytokine concentrations were determined in 26 patients with Guillain-Barre syndrome undergoing plasma exchange, 25 with other acute neurological diseases, and 40 healthy controls. Raised TNF-a concentrations (> 25 pg/ml) were found in seven of 26 patients with Guillain-Barre syndrome v none of 23 disease controls (p = 0 001). The peak grade of clinical deficit correlated with TNF-α concentrations (r = 0'6, p < 0-01). There was no significant difference between interleukin-1/β or interferon-y concentrations in patients and disease controls. The data suggest that TNF-a may be a critical factor in the pathogenesis of Guillain-Barre' syndrome.