TY - JOUR
T1 - The role of IL-12 and TNF-α in AIDP and AMAN
AU - Deng, H.
AU - Yang, X.
AU - Jin, T.
AU - Wu, J.
AU - Hu, L. S.
AU - Chang, M.
AU - Sun, X. J.
AU - Adem, A.
AU - Winblad, B.
AU - Zhu, J.
PY - 2008/10
Y1 - 2008/10
N2 - 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.
AB - 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.
KW - Guillain-Barré syndrome
KW - Interleukin 12
KW - Intravenous high dose immunoglobulin
KW - Receptors
KW - Tumour necrosis factor
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U2 - 10.1111/j.1468-1331.2008.02261.x
DO - 10.1111/j.1468-1331.2008.02261.x
M3 - Article
C2 - 18717726
AN - SCOPUS:51349128257
SN - 1351-5101
VL - 15
SP - 1100
EP - 1105
JO - European Journal of Neurology
JF - European Journal of Neurology
IS - 10
ER -