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The role of IL‐12 and TNF‐α in AIDP and AMAN
Author(s) -
Deng H.,
Yang X.,
Jin T.,
Wu J.,
Hu L.S.,
Chang M.,
Sun X.J.,
Adem A.,
Winblad B.,
Zhu J.
Publication year - 2008
Publication title -
european journal of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.881
H-Index - 124
eISSN - 1468-1331
pISSN - 1351-5101
DOI - 10.1111/j.1468-1331.2008.02261.x
Subject(s) - medicine , acute motor axonal neuropathy , tumor necrosis factor alpha , pathogenesis , peripheral blood mononuclear cell , guillain barre syndrome , polyradiculoneuropathy , immunology , immune system , biology , biochemistry , in vitro
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.