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At the cellular level, endothelial cell activation and apoptosis are initiated by the deposition of immune complexes containing scleroderma-specific antibodies leading to the activation of toll-like receptors (TLR), amplifying inflammatory pathways, including nuclear factor kappa B (NFκB), p38 mitogen-activated protein kinase (p38MAPK), and stress-activated protein kinases (SAPK)/jun amino-terminal kinases (JNK), as well as upregulating adhesion molecules like intercellular adhesion molecule-1 (ICAM-1) and pro-inflammatory cytokines like interleukin (IL)-6 and IL-8, leading to inflammatory cell recruitment within the vasculature, leading to swelling and lymphohistiocytic infiltrate [4]
