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Hartung, H.P. et al.

The role of interferon-gamma in the pathogenesis of experimental autoimmune disease of the peripheral nervous system.

The role of interferon-gamma in the pathogenesis of experimental autoimmune disease of the peripheral nervous system was investigated. Administration of rat recombinant interferon-gamma markedly augmented both myelin-induced and T-cell line-mediated experimental autoimmune neuritis. Conversely, in vivo application of a monoclonal antibody to interferon-gamma suppressed the disease. Clinical and electrophysiological findings were corroborated by semiquantitative morphometric analysis. Mechanisms responsible for the enhancing effects of interferon-gamma include upregulation of major histocompatibility complex class II antigen expression in the nerve lesion, increased cellular influx of T cells and macrophages, and heightened macrophage activity with enhanced release of toxic oxygen species. These observations establish a pivotal role of the cytokine interferon-gamma in the pathogenesis of experimental autoimmune disease of the peripheral nervous system.[1]

References

The role of interferon-gamma in the pathogenesis of experimental autoimmune disease of the peripheral nervous system. Hartung, H.P., Schäfer, B., van der Meide, P.H., Fierz, W., Heininger, K., Toyka, K.V. Ann. Neurol. (1990) [Pubmed]

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