Stat4 Isoforms Differentially Regulate Inflammation and Demyelination in Experimental Allergic Encephalomyelitis

Experimental Allergic Encephalomyelitis Inflammation and Demyelination in Stat4 Isoforms Differentially Regulate

Demyelination and neurological signs in experimental allergic encephalomyelitis.

Because of the reported absence of demyelination in some animals with neurological signs of experimental allergic encephalomyelitis (EAE), it has been suggested that these signs are not due to demyelination. The present study demonstrates that there is ample demyelination in the central nervous system (CNS) and peripheral nervous system (PNS) to account for the neurological signs in rats with m...

A Novel MRI Texture Analysis of Demyelination and Inflammation in Relapsing-Remitting Experimental Allergic Encephalomyelitis

We have developed a novel multiscale localized image texture analysis technique, based upon the polar Stockwell Transform (PST). In this paper we characterized image texture in vivo using the PST in histologically verified lesion areas in T2-weighted MRI of an animal model of multiple sclerosis. Both high and low frequency signals, representing inflammation and demyelination, were significantly...

nerve growth factor prevents demyelination, cell death and progression of the disease in experimental allergic encephalomyelitis

experimental allergic encephalomyelitis (eae), a demyelinating disease induced in the animals parallels multiple sclerosis in human in several aspects, provides a useful model to investigate multiple sclerosis. in this study, we have therefore used this model to study functions of nerve growth factor (ngf) in eae. ngf with considerable effects on neuron survival, proliferation and differentiati...

STAT4 isoforms differentially regulate Th1 cytokine production and the severity of inflammatory bowel disease.

STAT4, a critical regulator of inflammation in vivo, can be expressed as two alternative splice forms, a full-length STAT4alpha, and a STAT4beta isoform lacking a C-terminal transactivation domain. Each isoform is sufficient to program Th1 development through both common and distinct subsets of target genes. However, the ability of these isoforms to mediate inflammation in vivo has not been exa...