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Experimental allergic encephalomyelitis (EAE) is a CNS autoimmune disease mediated by the action of CD4(+) T cells, macrophages, and proinflammatory cytokines. IL-10 is a cytokine shown to have many anti-inflammatory properties. Studies have shown both inhibition and exacerbation of EAE after systemic IL-10 protein administration. We have compared the inhibitory effect in EAE of Il10 gene delivery in the CNS. Fibroblasts transduced with retroviral vectors expressing IL-10 could inhibit EAE. This was not associated with a prevention of cellular recruitment but an alteration in their phenotype, notably an increase in the numbers of CD8(+) T and B cells. In marked contrast, CNS delivery of adenovirus coding for mouse IL-10 or IL-10 protein performed over a wide dose range failed to inhibit disease, despite producing similar or greater amounts of IL-10 protein. Thus the action of IL-10 may differ depending on the local cytokine microenvironment produced by the gene-secreting cell types.

Original publication

DOI

10.4049/jimmunol.166.6.4124

Type

Journal article

Journal

Journal of immunology (Baltimore, Md. : 1950)

Publication Date

03/2001

Volume

166

Pages

4124 - 4130

Addresses

Neuroinflammation Group, Department of Neurochemistry, Institutes of Neurology and Ophthalmology, UCL, University of London, London, United Kingdom. jcroxfor@hgmp.mrc.ac.uk

Keywords

Spinal Cord, Cell Line, Transformed, Fibroblasts, Animals, Mice, Inbred Strains, Mice, Adenoviridae, Retroviridae, Encephalomyelitis, Autoimmune, Experimental, Nerve Tissue Proteins, Interleukin-10, Histocompatibility Antigens Class II, CD4-CD8 Ratio, Injections, Intraventricular, Injections, Subcutaneous, Temperature, Cell Movement, Down-Regulation, Genetic Vectors, Genetic Therapy