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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Myocytes respond to both interleukin-4 and interferon-gamma: cytokine responsiveness with the potential to influence the severity and course of experimental myasthenia gravis.

Messenger RNA that encodes for interleukin-15 (IL-15) has been reported to be constitutively expressed in skeletal muscle, although the protein product is not generally observed. Furthermore, interferon-gamma (IFN-gamma) has been reported to exacerbate symptoms of experimental myasthenia gravis (EAMG). Therefore, since IL-15 is an activator of IFN-gamma-producing cells, the hypothesis that drove the study reported below proposes that muscle is not a passive participant in the development of disease symptoms in EAMG and, in fact, plays a very important active role by producing immunomodulating factors that can influence the eventual immunopathological impact of the immune system on muscle. Tests of this hypothesis, made using a monoclonal skeletal myocyte line from the Lewis rat, have indicated that myocytes produce IL-15 protein following exposure to interleukin-4 (IL-4), an interesting paradox in light of the usual anti-inflammatory role played by IL-4. Furthermore, the level of IL-15 also can be regulated by IFN-gamma itself. Although yet to be confirmed in vivo, IFN-gamma has been shown to be capable of activating cultured myocytes in a variety of ways that could influence the ongoing autoimmune response associated with EAMG.[1]

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