Journal of the neurological sciences · 2010
Clinical study on CXCL13, CCL17, CCL20 and IL-17 as immune cell migration navigators in relapsing-remitting multiple sclerosis patients.
Контролируемое клиническое исследованиеСтатьяНазвание и аннотация: Перевод пока не подготовлен
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Kalinowska-Łyszczarz Alicja, Szczuciński Adam, Pawlak Mikołaj A, Losy Jacek
Аннотация
BACKGROUND: There has been a growing evidence for the role of chemokines in the pathology of multiple sclerosis. Recently, there has been great emphasis placed on humoral immunity and the T(H)-17 response, which has not yet been thoroughly described in MS. The aim of this study was to investigate the role of specific chemokines involved in B-cell migration (CXCL13) and in the T(H)-17 immune response (IL-17, CCL17, CCL20).
METHODS: Using ELISA, the chosen chemokine concentrations were measured in the serum and cerebrospinal fluid of relapsing-remitting MS patients with both active and stable disease, and the relapse prediction rate was calculated.
RESULTS: We found that the CSF concentrations of CXCL13 in patients with RRMS both, during relapse and remission, were significantly higher than in controls. CCL17 and CCL20 were not detected in CSF in either of the groups, whereas serum CCL20 level was significantly higher in remission than during relapse. Intravenous methylprednisolone treatment of patients with relapse did not influence serum CXCL13 and CCL20 levels. However, it did lower CCL17 and IL-17 concentrations.
CONCLUSIONS: CXCL13 is an important mediator in MS that is strongly linked to the neuroinflammatory activity of the disease. However, more studies are needed for elucidating the roles of CCL17, CCL20 and IL-17 in MS pathology.
METHODS: Using ELISA, the chosen chemokine concentrations were measured in the serum and cerebrospinal fluid of relapsing-remitting MS patients with both active and stable disease, and the relapse prediction rate was calculated.
RESULTS: We found that the CSF concentrations of CXCL13 in patients with RRMS both, during relapse and remission, were significantly higher than in controls. CCL17 and CCL20 were not detected in CSF in either of the groups, whereas serum CCL20 level was significantly higher in remission than during relapse. Intravenous methylprednisolone treatment of patients with relapse did not influence serum CXCL13 and CCL20 levels. However, it did lower CCL17 and IL-17 concentrations.
CONCLUSIONS: CXCL13 is an important mediator in MS that is strongly linked to the neuroinflammatory activity of the disease. However, more studies are needed for elucidating the roles of CCL17, CCL20 and IL-17 in MS pathology.