Cytokines play an important role in the pathogenesis of autoimmune diseases including Guillain-Barré syndrome (GBS) and its animal model experimental autoimmune neuritis (EAN). In this article, we reviewed the current knowledge of the role of cytokines such as TNF-α, IFN-γ, IL-1β, IL-6, IL-12, IL-18, IL-23, IL-17, IL-10, IL-4 and chemokines in GBS and EAN as unraveled by studies both in the clinic and the laboratory. However, these studies occasionally yield conflicting results, highlighting the complex role that cytokines play in the disease process. Efforts to modulate cytokine function in GBS and other autoimmune disease have shown efficiency indicating that cytokines are important therapeutic targets.

Chemokines and their receptors have been strongly implicated in the inflammatory process and pathogenesis of the neurodegenerative disorders, such as Alzheimer's disease (AD). In the present study, we examined the expression of chemokines, fractalkine, interferon-inducible protein-10 (IP-10) and macrophage inflammatory protein-1a (MIP-1a) by immunohistochemistry in the brain of transgenic mice APP SWE (Tg2576) at ages of 9, 11, and 17 months, which over-express a mutated form of human amyloid precursor protein (APP). Decreased fractalkine and increased IP-10 expression in cerebral cortex and hippocampus were found at ages of 9 and 17 months in Tg2576 mice when compared with agematched control mice. On the contrary, MIP-1a expression showed no difference between Tg2576 mice and aged controls and was not influenced by ages. b-amyloid (Ab) positive plaques were co-located with the intense IP-10 expression. The finding suggests fractalkine and IP-10 may participate in the pathogenesis of AD; and could be new therapeutic strategies for neuroprotection.

The exact role of TNF-alpha in excitotoxic neurodegeneration of the brain is unclear. To address this issue, the kainic acid (KA)-induced hippocampal injury model, a well-characterized model of human neurodegenerative diseases, was used in TNF-alpha receptor 1 (TNFR1)-knockout (TNFR1-/-) mice in the present study. After nasal application of a single dose of 40 mg of KA per kilogram body weight, TNFR1-/- mice showed significantly more severe seizures than the wild-type mice. In addition, obvious neurodegeneration, enhanced microglia activation, and astrogliosis in the hippocampus, as well as increased locomotor activity, were found in TNFR1-/- mice compared with the wild-type controls 8 days after KA delivery. Moreover, CC chemokine receptor 3 expression on activated microglia was increased 3 days after KA treatment in TNFR1-/- mice, as measured by flow cytometry. These data suggest that TNF-alpha may play a protective role through TNFR1 signaling.