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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




Journal article


Journal of immunology (Baltimore, Md. : 1950)

Publication Date





4124 - 4130


Neuroinflammation Group, Department of Neurochemistry, Institutes of Neurology and Ophthalmology, UCL, University of London, London, United Kingdom.


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