Dr Jie Zhu, Division of Neurodegeneration (NOVUM, Plan 5), Department of Neurobiology, Care Sciences and Society, Karolinska Institute, Karolinska University Hospital in Huddinge, Stockholm SE-141 86, Sweden (tel.: +46 8 58585494; fax: +46 8 58585470; e-mail: [email protected]).

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Abstract

Background: Acute inflammatory demyelinating polyradiculoneuropathy (AIDP) and acute motor axonal neuropathy (AMAN) have been described as two major subtypes of Guillain-Barré syndrome (GBS); however, the possible difference of their immune-inflammatory pathogenesis remains unclear.

Methods: In this study, by using FACS and enzyme-linked immunosorbent assays analyses, the role of Th1 cytokines tumour necrosis factor-α (TNF-α), interleukin-12 (IL-12) and their receptors on peripheral blood mononuclear cells (PBMCs) and in serum concentrations were investigated in AIDP and AMAN.

Results: The results showed enhanced IL-12, IL-12R1 in AIDP and TNF-α in AMAN during the acute phase, as well as increased TNF-α and TNFR1 during the plateau phase of AIDP. Intravenous high dose immunoglobulin decreased IL-12R1 expression on cells in AIDP, but increased TNF-α and TNFR2 in AMAN.

Discussion: Our data suggest that IL-12 promotes disease development in AIDP and in contrast to previously inflammatory assumptions, TNF-α may play double roles in GBS. The anti-inflammatory role of TNF-α realized through TNFR2 in AMAN is possibly a therapeutic mechanism in the IVIg treatment of AMAN.

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Volume15, Issue10

October 2008

Pages 1100-1105

The role of IL-12 and TNF-α in AIDP and AMAN

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The role of IL-12 and TNF-α in AIDP and AMAN

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