Multiple Sclerosis, 1 October 2003, vol. 9, no. 5, pp. 440-445(6)
Jansson A.; Ernerudh J.; Kvarnström M.; Ekerfelt C.; Vrethem M.
 Clinical Research Centre and Department of Molecular and Clinical Medicine, Division of Clinical Immunology, Linköping University, S-581 85 Linköping, Sweden  Clinical Research Centre and Department of Molecular and Clinical Medicine, Division of Clinical Immunology, Linköping University, S-581 85 Linköping, Sweden  Department of Neuroscience and Locomotion, Division of Neurology and Neurophysiology, Faculty of Health Sciences, Linköping University, S-581 85 Linköping, Sweden
The mechanisms behind the beneficial effects of interferon-ß1a (IFN-ß1a) and glatiramer acetate (GA) in the treatment of multiple sclerosis (MS) are still uncertain.
Altered cytokine patterns have been suggested including inhibition of proinflammatory cytokines like interferon-g (IFN-g) and enhancement of anti-inflammatory cytokines such as interleukin-4 (IL-4).
Twenty-nine patients with MS (10 untreated, nine treated with IFN-ß1a and 10 with GA) were investigated with elispot of peripheral blood mononuclear cells.
Spontaneous and myelin induced (myelin basic protein (MBP), myelin oligodendrocyte glycoprotein (MOG)-14-39 and MOG 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 MOG 14-39 induced IL-4 secretion in the IFN-1a treated group.
Thus, immunological effects of IFN-ß1a and GA were similar showing that disease promoting Th1 (IFN-g) cells were reduced while the potentially beneficial Th2 response (IL-4) was maintained.