This work shed new light on the role of TG2 in the endothelium where the extracellular pool of TG2 is involved in regulating cell-matrix adhesion while the cytoplasmic TG2 is important for cell cycle progression and survival. Furthermore, it was shown that CD IgA antibodies disturb the extracellular function of TG2, thus altering endothelial cell-extracellular matrix (ECM) interactions and thereby affecting endothelial cell adhesion, polarization and motility. Intriguingly, CD IgA promoted the secretion of the redox sensor protein TRX, which probably is needed to keep TG2 in a conformation suitable for the constitutive antibody binding and activation. Thus, this study set up a possible molecular mechanism by which CD antibodies exert their anti-angiogenic functions, which in turn might help to explain the altered small-bowel mucosal microvasculature observed in untreated CD patients.
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