Elispot assay detection of cytokine secretion in multiple sclerosis patients treated with interferon-b1a or glatiramer acetate compared with untreated patients

Author:

Jansson A1,Ernerudh J1,Kvarnström M1,Ekerfelt C1,Vrethem M2

Affiliation:

1. Clinical Research Centre and Department of Molecular and Clinical Medicine, Division of Clinical Immunology, Linköping University, S-581 85 Linköping, Sweden

2. Department of Neuroscience and Locomotion, Division of Neurology and Neurophysiology, Faculty of Health Sciences, Linköping University, S-581 85 Linköping, Sweden,

Abstract

The mechanisms behind the beneficial effects of interferon-b1a (IFN-b1a) and glatiramer acetate (GA) in the treatment of multiple sclerosis (MS) are still uncertain. A ltered cytokine patterns have been suggested including inhibition of proinflammatory cytokines like interferon-g (IFN-g) and enhancement of anti-inflammato ry cytokines such as interleukin-4 (IL-4). Twenty-nine patients with MS (10 untreated, nine treated with IFN-b1a and 10 with GA) were investigated with elispot of peripheral blood mononuclear cells. Spontaneous and myelin induced (myelin basic protein (MBP), myelin oligodendro cyte glycoprotein (MO G)-14-39 and MO G 63-87) IFN-g, IL-4, IL-5 and IL-10 secretion was studied. We found a significant reduction of spontaneous IFN-g, IL-4 and IL-5, but no difference in IL-10 secreting cells in both groups of treated patients compared with the untreated patients. Myelin-specific responses showed a significant decrease of IFN-g and an increase of IL-5, but no change in IL-4 and IL-10 secreting cells in treated compared with untreated patients. Both treatment groups revealed similar cytokine secretion patterns except for a more pronounced decrease of both spontaneous and MO G 14-39 induced IL-4 secretion in the IFN-b1a treated group. Thus, immunological effects of IFN-b1a and G A were similar showing that disease promoting Th1 (IFN-g) cells were reduced while the potentially beneficial Th2 response (IL-4) was maintained.

Publisher

SAGE Publications

Subject

Neurology (clinical),Neurology

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