Preferential increase of B-cell activating factor in the cerebrospinal fluid of neuromyelitis optica in a white population

Multiple Sclerosis Journal - Tập 16 Số 12 - Trang 1453-1457 - 2010
Adi Vaknin‐Dembinsky1, Livnat Brill1, Naama Orpaz1, Oded Abramsky1, Dimitrios Karussis1
1Department of Neurology and Laboratory of Neuroimmunology and the Agnes-Ginges Center for Neurogenetics, Hadassah-Hebrew University Hospital, Ein-Karem, Jerusalem, Israel,

Tóm tắt

Background: Anti-aquaporin-4 antibodies are believed to have a central pathogenetic role in neuromyelitis optica (NMO). B-cell activating factor (BAFF) is one of the crucial factors that determines the fate and survival of B cells and may play a role in induction of antibody-mediated autoimmunity. Objectives: To evaluate the blood and cerebrospinal fluid (CSF) levels of BAFF in NMO and multiple sclerosis (MS) patients. Methods: Peripheral blood samples were collected from 21 definite NMO patients, 22 healthy controls and 45 MS patients and CSF from 8 NMO and 11 MS patients. BAFF levels were measured using an ELISA technique. Results: We found significantly higher levels of BAFF in the CSF of NMO patients compared with that in MS (215.6 ± 41 pg/ml in NMO and 77.4 ± 11 pg/ml in MS, p < 0.001). There were no differences in serum BAFF levels between NMO, MS and healthy donors. MS patients treated with interferon-beta (IFNβ) or glatiramer acetate (GA) had significantly higher serum BAFF levels, as compared with untreated patients (1227 ± 203 pg/ml in untreated MS, 2253 ± 83.4 pg/ml in GA-treated, p < 0.01, and 2106 ± 277.9 pg/ml in interferon-treated, p < 0.05) Conclusion: The presence of increased BAFF, a soluble factor associated with B-cell activation in the proximity of the disease target organ (CSF) in NMO, and its increase in association with immunomodulating treatments, may help our understanding of the immunopathogenetic mechanisms involved in this disease and contribute to more successful and targeted therapeutic intervention.

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Tài liệu tham khảo

10.1016/j.jneuroim.2006.06.032

10.1111/j.1749-6632.2009.04871.x

10.1038/nri2572

10.1172/JCI0214121

10.1002/1529-0131(200106)44:6<1313::AID-ART223>3.0.CO;2-S

10.1093/brain/awn077

10.1212/01.wnl.0000216139.44259.74

10.1212/WNL.0b013e3181c919ee

10.1177/1352458509106228

10.1001/archneurol.2007.17

10.1177/1352458507084107

10.1093/brain/awl371

10.1016/j.it.2007.01.005

Duddy M., 2006, Int MS J, 13, 84

10.1016/j.jneuroim.2010.01.009

Speciale L., 2000, J Neurovirol, 6, S57