IL-10 and IFN-gamma in Guillain-Barre syndrome

Citation
R. Press et al., IL-10 and IFN-gamma in Guillain-Barre syndrome, J NEUROIMM, 112(1-2), 2001, pp. 129-138
Citations number
27
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROIMMUNOLOGY
ISSN journal
01655728 → ACNP
Volume
112
Issue
1-2
Year of publication
2001
Pages
129 - 138
Database
ISI
SICI code
0165-5728(20010101)112:1-2<129:IAIIGS>2.0.ZU;2-#
Abstract
Guillain-Barre syndrome (GBS) is an acute inflammatory disease affecting my elin and axons of the peripheral nervous system (PNS). GBS is considered to be caused by breakdown of tolerance to autoantigens of the PNS. The involv ement of cytokines in GBS and in relation to treatment with high dose intra venous immunoglobulin (IvIg) is incompletely known. We studied the temporal profiles of IL-10 and IFN-gamma -secreting blood mononuclear cells (MNC) o ver the course of GBS, using enzyme-linked immunospot (ELISPOT) assays. Pre treatment levels of blood MNC spontaneously secreting IL-10 were higher in the acute phase of GBS than in control patients with aseptic meningitis, ot her neurological diseases, diabetic neuropathy and healthy subjects. Levels of IFN-gamma -secreting blood MNC were not increased over the course of GB S. Patients treated with IvIg had lower numbers of IL-10-secreting MNC comp ared to untreated patients. High levels of IL-10-secreting MNC correlated w ith serum anti-ganglioside IgM antibody levels, and with neurophysiological signs of axonal damage. The present data suggests that IFN-gamma is not in volved in GBS pathogenesis, and IL-10 being up-regulated in the early phase of GBS and associated with axonal damage, may have a pathogenetic role in GBS. (C) 2001 Elsevier Science B.V. All rights reserved.