The role of IL-12 and TNF-alpha in AIDP and AMAN
Autor(es): Deng H,Yang X,Jin T,Wu J,Hu L-S,Chang M,Sun X-J,Adem A,Winblad B,Zhu J
Resumo: 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. 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. 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. 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.
Palavras-Chave: Guillain-Barre syndrome; Interleukin 12; Intravenous high dose immunoglobulin; Receptors; Tumour necrosis factor
Imprenta: European Journal of Neurology, v. 15, n. 10, p. 1100-1105, 2008
Identificador do objeto digital: 10.1111/j.1468-1331.2008.02261.x
Descritores: Guillain-Barre Syndrome - Biosynthesis ; Guillain-Barre Syndrome - Cell ; Guillain-Barre Syndrome - Pathogenesis ; Guillain-Barre Syndrome - Protein synthesis ; Guillain-Barre Syndrome - Proteins ; Guillain-Barre Syndrome - Antibodies ; Guillain-Barre Syndrome - Cytokines
Data de publicação: 2008
