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This includes proposed up-regulation of endothelial nitric oxide synthase (NOS3), decreased stimulation of endothelial cells, development of anti-oxidative responses, decreased migration of inflammatory cells, decreased antigen presentation because of suppressed MHC II expression in endothelial cells [57] resulting from promoter IV of class II trans-activator (CIITA) [58], down-regulation of pro-inflammatory cytokines, decreased PLT accumulation, development of 15-epi-lipoxin (15-epi-LXB4), which operates through preventing the signaling pathways engaged in the stimulation of the inflammatory response induced by lipid agents [59, 60] and, finally, enhanced migration, differentiation, and prohibitory functions of Treg cells [59, 61]

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(2023f, December 15)

Thyroid Stimulating Hormone Receptor Antibody (TRAb) is the primary immunological characteristic of GD (2, 3)