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

H. Deng, X. Yang, T. Jin, J. Wu, L. S. Hu, M. Chang, X. J. Sun, A. Adem, B. Winblad, J. Zhu

Research output: Contribution to journalArticlepeer-review

26 Scopus citations


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.

Original languageBritish English
Pages (from-to)1100-1105
Number of pages6
JournalEuropean Journal of Neurology
Issue number10
StatePublished - Oct 2008


  • Guillain-Barré syndrome
  • Interleukin 12
  • Intravenous high dose immunoglobulin
  • Receptors
  • Tumour necrosis factor


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