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Different Therapeutic Outcomes in Experimental Allergic Encephalomyelitis Dependant Upon the Mode of Delivery of IL-10: A Comparison of the Effects of Protein, Adenoviral or Retroviral IL-10 Delivery into the Central Nervous System¹

J. Ludovic Croxford^2,*, Marc Feldmann, Yuti Chernajovsky and David Baker^*

^* Neuroinflammation Group, Department of Neurochemistry, Institutes of Neurology and Ophthalmology, UCL, Kennedy Institute of Rheumatology, Imperial College, and Bone and Joint Research Unit, Queen Mary and Westfield College, University of London, London, United Kingdom

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.

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