Does amyloid-beta 25-35 peptide induce expression of monoamine oxidase B in cultured rat astrocytes?
A beta 25-35 is able to selectively induce MAO-B expression in rat astrocytes and that the upregulation of MAO-B in A beta 25-35-stimulated astrocytes may play an important role in the pathogenesis of Alzheimer's disease.
Our data indicate that immunomodulatory molecules such as PD-L1 rather than Tregs play pivotal roles in the tissue-specific regulation of alloresponses. Further studies are needed to refine the significance of the PD-L1 pathway in GVHD and its versatility for therapeutic intervention.