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Mature oligodendrocytes create myelin by enveloping axons with their very own cell membrane in a spiral shape, which at some point becomes a multilayered sheath covering a extended segment of axon (Nave 2010). In the CNS, compact myelin has been shown by electron microscopy to possess a periodic ultrastructure which needs the expression of structural proteins which include MBP, myelin oligodendrocyte glycoprotein (MOG), and proteolipid protein. The functions of most myelin-associated proteins, which have only lately been identified by proteomics ( Jahn and other people 2009), are usually not well understood. It's clear that that they will be presented as Ags and that autoreactive T cells particular to these and also other less well-studied Ags play a crucial role in driving demyelinating pathogenesis. Despite the fact that oligodendrocytes make and include myelin, they cannot present it as an Ag to pathogenic CD4 + T cells simply because they do not constitutively express MHC class II (Wong and other folks 1984) and cannot be induced to in vitro either. Nevertheless, they likely play a substantial part inside the release of self-Ags for the capture and presentation by neighboring microglia. Although oligodendrocytes aren't believed to secrete cytokines to initiate an immune response, they do have the capability to respond to cytokines in their microenvironment. One example is, each IL-1b and IL-1b receptor are constitutively expressed in the CNS by oligodendrocytes and IL-1b inhibits OPC proliferation and enhances the VT-464 site survival of mature MBP + oligodendrocytes (Vela and other people 2002). IL-6R is present on oligodendrocytes and binding of IL-6 supports oligodendrocyte differentiation and survival (Pizzi and other folks 2004, Valerio and others 2002). Of certain interest, IFN-g protects against myelin harm inside a cuprizone-induced demyelination animal model (Gao and other folks 2000), whereas ectopic overexpression of IFN-g inside the retina protects against neurotropic viral infections but results in CNS demyelination (Geiger and other folks 1994), while the precise mechanism of this differential protection remains undetermined.759 II molecules in vivo or in vitro; on the other hand, they will be induced to complete so ( Jemison and other folks 1993; Prat and other folks 2000). Furthermore, murine brain endothelial cells are reported to course of action and present MBP and may induce the proliferation of sensitized T cells (McCarron and other folks 1986). The inducibility of MHC II molecules on brain endothelium by IFN-g has been linked to the activation with the MHC-II transactivator (CIITA) and seems to correlate with EAE susceptibility (Nikcevich and other people 1997). In EAE, expression of MHC II molecules on endothelial cells increases before immune cell infiltration with the brain (Sobel and others 1984), suggesting that this may be a important event throughout brain inflammation. Human and mouse endothelial cells express B7 molecules in culture when stimulated with IFN-g (Prat and other folks 2000). Having said that, two unique labs each failed to induce T cell proliferation with brain endothelial cells in two various models of Ag presentation (Risau and other people 1990; Prat and other individuals 2000). It's effectively established that T cells invade tissues by extravasating through vascular endothelial cells through integrin receptors which include VCAM-1; thus, it is actually this interaction that may be targeted by the MS drug natalizumab.