HIGHLIGHTS
SUMMARY
Previous studies have shown the presence of Abs against AT1R (AT1R-Abs) and ETAR (ETAR-Abs) in solid organ transplant recipients with chronic allograft dysfunction, thus raising significant concerns for the direct pathogenetic effect of Abs in the process of chronic rejection. AT1R-Abs and ETAR-Abs do not activate complement or mediate opsonization and are therefore not harmful to receptor expressing cells. AT1R-Abs and ETAR-Abs activate only the main receptors AT1R and ETAR, resulting in skewing of receptor activation and in disruption of normal homeostasis. The exact mechanisms as well as . . .
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