More MS news articles for Nov 2001

Treatment with Anti-interferon-gamma Monoclonal Antibodies Modifies Experimental Autoimmune Encephalomyelitis in Interferon-gamma Receptor Knockout Mice

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11716570&dopt=Abstract

Exp Neurol 2001 Dec;172(2):460-8
Espejo C, Penkowa M, Saez-Torres I, Xaus J, Celada A, Montalban X, Martinez-Caceres EM.
Unitat de Neuroimmunologia Clinica, Hospital Vall d'Hebron, Barcelona, 08035, Spain

The role of interferon-gamma (IFN-gamma) in the pathogenesis of multiple sclerosis and experimental autoimmune encephalomyelitis (EAE) is still controversial.

We have studied the function of IFN-gamma and its receptor in the EAE model using two different IFN-gamma receptor knockout (IFN-gamma R(-/-)) mouse types: C57Bl/6x129Sv, with a disruption of the IFN-gamma receptor cytoplasmic domain, and 129Sv, homozygous for a disrupted IFN-gamma receptor gene.

Mice were immunized with peptide 40-55 from rat myelin oligodendrocyte glycoprotein.

A subgroup of mice was treated with anti-IFN-gamma monoclonal antibodies (mAb) on day 8 postimmunization.

Clinical scoring and both histological and immunohistochemical studies were undertaken for all groups.

We hereby show that treatment with anti-IFN-gamma mAb worsened the disease course of 129Sv wild-type mice.

However, it decreased the mean daily score in IFN-gamma R(-/-) 129Sv and the incidence of the disease down to 50% in C57Bl/6x129Sv IFN-gamma R(-/-) mice.

Moreover, after anti-IFN-gamma mAb treatment, oxidative stress levels, metallothionein I and II antioxidant protein expression, and apoptoticneuronal death were increased in wild-type mice while decreased in IFN-gamma R(-/-) mice.

These results suggest a putative alternative mechanism of action of this cytokine that works independent of its receptor.
 

PMID: 11716570 [PubMed - in process]

(c) 2001 Elsevier Science