The role of IL-12 and TNF-alpha 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-alpha (TNF-alpha), 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-alpha in AMAN during the acute phase, as well as increased TNF-alpha and TNFR1 during the plateau phase of AIDP. Intravenous high dose immunoglobulin decreased IL-12R1 expression on cells in AIDP, but increased TNF-alpha and TNFR2 in AMAN.


CONCLUSIONS
Our data suggest that IL-12 promotes disease development in AIDP and in contrast to previously inflammatory assumptions, TNF-alpha may play double roles in GBS. The anti-inflammatory role of TNF-alpha realized through TNFR2 in AMAN is possibly a therapeutic mechanism in the IVIg treatment of AMAN.
Deng
H
H
Department of Neurology, The First Hospital, Jilin University, Changchun, China.
Yang
X
X
Jin
T
T
Wu
J
J
Hu
L-S
LS
Chang
M
M
Sun
X-J
XJ
Adem
A
A
Winblad
B
B
Zhu
J
J
D000208:Acute Disease; D000293:Adolescent; D000328:Adult; D018450:Disease Progression; D005260:Female; D005786:Gene Expression Regulation; D020275:Guillain-Barre Syndrome / Q000097:blood / Q000145:classification / Q000503:physiopathology* / Q000628:therapy; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000494:pharmacology / Q000627:therapeutic use; D018664:Interleukin-12 / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*; D007963:Leukocytes, Mononuclear / Q000737:chemistry; D008297:Male; D008875:Middle Aged; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D047889:Receptors, Tumor Necrosis Factor, Type II / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000235:genetics / Q000502:physiology*
D016756:Immunoglobulins, Intravenous; D047888:Receptors, Tumor Necrosis Factor, Type I; D047889:Receptors, Tumor Necrosis Factor, Type II; C415902:TNFRSF1B protein, human; D014409:Tumor Necrosis Factor-alpha; D018664:Interleukin-12