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

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.