Abstract
Interferon (IFN) was originally discovered in 1958, when it was found that extracts of virally infected cells conferred anti-viral resistance in host cells.1 Since the discovery of IFN, it has become clear that there are at least three antigenically defined families of IFNs (IFN-β, IFN-γ, and IFN-α) and that such IFNs have diverse, pleiotropic effects on IFN receptor-bearing host cells.2-3 Some of these host cell effects include the modulation of cell growth and the induction of antigens of the Major Histocompatibility Complex (MHC). The ability of IFN s to stimulate the expression of MHC antigens suggests that they could be involved in the immunopathological responses of tissues to disease or injury. This may be the case for the destruction of islet γ cells in the diabetic pancreas4 or demyelination of CNS neurons in multiple sclerosis.5 In this chapter, however, the ability of CNS cells to produce (and, or make biological responses to) IFN in the context of normal developmental processes and proliferation will be used as a model to illustrate the scope for IFN action. Studies of CNS injury and development at the molecular level might have implications for similar functions in the pancreas.6
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Tedeschi, B. (1992). Interferon — A Candidate Mediator of Cell Growth. In: Vinik, A.I., Sirman, D.J. (eds) Pancreatic Islet Cell Regeneration and Growth. Advances in Experimental Medicine and Biology, vol 321. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-3448-8_7
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DOI: https://doi.org/10.1007/978-1-4615-3448-8_7
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