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Similar evidence originates from experimental arthritis, diabetes and multiple sclerosis models, further highlighting the crucial role of the Tregs in controlling the delicate balance between tolerance and autoimmunity.
Therefore, ADAM17 blockers have been used in rheumatoid arthritis and multiple sclerosis models to reduce the production of sTNF- α in order to decrease inflammation.
Functional recovery of axons during treatments of multiple sclerosis models has not been previously addressed using such a combination of complementary modalities.
For instance, blockade of the inducible costimulator (ICOS) is therapeutic in CIA but augments disease in diabetes and some multiple sclerosis models [ 32].
Thank you for submitting your work entitled "A pain-mediated neural signal induces relapse in multiple sclerosis models" for peer review at eLife.
VGSC blockers such as TTX, lidocaine, procaine, mexiletine, phenytoin and carbamazepine protect against white matter axonal damage in multiple sclerosis models (Waxman et al., 1994 a ; Carter, 1998; Hewitt et al., 2001; Kapoor et al., 2003; Black and Waxman, 2008).
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Pulmonary delivery of soluble antigen arrays (SAgAs) was explored in mice with experimental autoimmune encephalomyelitis (EAE), a multiple sclerosis model.
In vitro dTNFR is as effective as etanercept-like molecules at inhibiting TNF-α activity [ 17] and has previously been shown to be therapeutic in both the CIA model [ 19, 47] and a multiple sclerosis model [ 48].
Interestingly, in the mouse EAE multiple sclerosis model, microglial activation occurs prior to monocyte-derived macrophage recruitment, suggesting that the kinetics are disease-cue dependent (Ajami et al., 2011).
At the same time, infiltrating monocyte-derived macrophages correlate well with tissue damage in the multiple sclerosis EAE model and meningitis mouse models.
In vitro data and experimental multiple sclerosis animal models provide evidence that mitochondrial injury can be induced by reactive oxygen and nitrogen species (Bolanos et al., 1997; Higgins et al., 2010; Witte et al., 2010; Nikić et al., 2011).
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