Acta Neurologica Scandinavica · 2010 · 103 citations · 21 references
Life SciencesImmunologyNeurologyAutoimmunityImmunopathologyNeuroimmunologyAmyotrophic Lateral SclerosisCentral Nervous System ImmunityCerebrospinal Fluid ImmunologyCytokine BiologyNeurodegenerative DiseasesNeuroinflammationAmyotrophic Lateral Sclerosis PathologyImmune-mediated PathogenesisImmunological MechanismsInterleukin-17 PathwayInterleukin-23 AxisT Helper 17 ImmunityTh17 Cell PathogenicityTh17 Responses
Rentzos M, Rombos A, Nikolaou C, Zoga M, Zouvelou V, Dimitrakopoulos A, Alexakis T, Tsoutsou A, Samakovli A, Michalopoulou M, Evdokimidis J. Interleukin-17 and interleukin-23 are elevated in serum and cerebrospinal fluid of patients with ALS: a reflection of Th17 cells activation?Acta Neurol Scand: 2010: 122: 425–429.© 2010 The Authors Journal compilation © 2010 Blackwell Munksgaard. Background – There is evidence that immunological factors may involved in pathogenetic mechanisms of amyotrophic lateral sclerosis (ALS). Th17 cells are characterized by predominant production of IL-17 and are suggested to be crucial in destructive autoimmunity. Interleukin-23 (IL-23) appears to play a supporting role in the continued stimulation and survival of Th17. Patients and methods – We measured by enzyme-like immunosorbent assay (ELISA) serum and cerebrospinal fluid (CSF) levels of IL-17 and IL-23 in 22 patients with ALS and 19 patients with other non-inflammatory neurological disorders (NIND) studied as a control group. IL-17 and IL-23 serum and CSF levels were also correlated with duration of the disease, the disability level and the clinical subtype of the disease onset in patients with ALS. Results – IL-17 and IL-23 serum levels were higher in patients with ALS as compared with patients with NIND (P = 0.015 and P = 0.002 respectively). IL-17 and IL-23 CSF levels were also increased in patients with ALS (P = 0.0006 and P = 0.000001 respectively). IL-17 and IL-23 levels were not correlated with disease duration, disability scale or clinical subtype of the disease onset in ALS patients. Conclusions – Our findings suggest that these molecules may be involved in the pathogenetic mechanisms acting as potential markers of Th17 cells activation in ALS.
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Immunologic reactions in amyotrophic lateral sclerosis brain and spinal cord tissue.
Toshio Kawamata, Haruhiko Akiyama, Tōru Yamada et al. · PubMed · 1992 · 546 citations