Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

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


J Immunol

Publication Date





4124 - 4130


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