TNFα promotes proliferation of oligodendrocyte progenitors and remyelination

By H. Arnett, J. Mason, M. Marino, Kinuko Suzuki, G. Matsushima, J. Ting. Nature Neuroscience, 2001

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How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Innate immunity: the missing link in neuroprotection and neurodegeneration? (2002, positive): “In an elegant study, Arnett et al.(38) used mice that lack TNF-α and its associated receptors to study demyelination and remyelination.”
Modulation of microglia can attenuate neuropathic pain symptoms and enhance morphine effectiveness. (2008, positive): “Although, TNF- has been implicated in the acceleration of injury, current studies suggest that TNF- may also serve a protective role [3, 24].”
Differentiation block of oligodendroglial progenitor cells as a cause for remyelination failure in chronic multiple sclerosis. (2008, background): “…pro-inflammatory cytokines (e.g. IL1b, TNF) results in impaired remyelination indicating that the inflammatory infiltrates create a beneficial environment for remyelination (Arnett et al., 2001; Mason et al., 2001; Bieber et al., 2003; Kotter et al., 2005; Chari et al., 2006; Setzu et al., 2006).”
TNF‐mediated inflammatory disease (2008, background): “In contrast, TNFR2 has been shown to promote proliferation of oligodendrocyte progenitors and remyelination in a neurotoxicant murine model of demyelination [130].”