Despite advancements in clinical management, treatment of patients with AIDP/GBS and its chronic variant CIDP remains palliative and relies on the use of non-specific immunemodulating therapies.
We examined sera of patients with Guillain-Barré syndrome (GBS), chronic inflammatory demyelinating polyradiculoneuropathy (CIDP), other neuropathies (ONP) and normal controls for IgM and IgG antibodies against PMP22 by ELISA (against synthetic PMP22 extracellular peptide fragments) and Western blot (against cauda equina).
T<sub>reg</sub> cell-mediated clinical response to IVIG therapy in GBS patients was associated with reciprocal regulation of effector T cells-expressing TNF-α.
DSCs showed a significant increase in IL-6 (p < 0.05), TNF-α (p < 0.05), IL-10 (p < 0.01), and TGF-β (p < 0.05) secretion after GBS infection, while these changes were not observed in infected ESCs.
Tumor necrosis factor-α (TNF-α), a proinflammatory cytokine, promotes transendothelial migration by upregulating endothelial expression of inflammatory mediators, including CCL2, a chemokine implicated in GBS.
Subgroup analysis further provided evidence of significant association between TNF-α308 G/A and risk of the GBS in Asian population (GG+GA vs. AA: OR=32, 95%CI=0.11-0.93; GG vs. AA: OR=0.32, 95%CI=0.15-0.68).
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 MMP9 C(-1562)T and TNFA C(-863)A SNP were associated with severe weakness and poor outcome, indicating that these SNP may be one of the factors predisposing to a severe form of GBS.