Abstract
Challenging and still unsolved problems in kidney transplantation are risk stratification and the treatment of humoral rejection. Antibody-mediated rejection is an important cause of early and chronic rejection. The impact of donor-specific HLA antibodies on antibody-mediated rejection–causing graft damage is well known, but the clinical relevance of non-HLA antibodies remains unclear. Recently, in 2 independent studies, a new correlation was found between the presence of non-HLA anti-Rho guanosine diphosphate dissociation inhibitor 2 (ARHGDIB) antibodies and increased graft failure. RhoGDI2, another name for ARHGDIB, is a negative regulator of the Rho guanosine triphosphate (RhoGTP)ases RhoA, Rac1m, and Cdc42, whose main function is regulating the actin network in a variety of cells. RhoGDI2 is mainly expressed intracellularly, and some expression is observed on the cell surface. Currently, there is no mechanism known to explain this correlation. Additionally, the reason why the antibodies are produced is unknown. In this review, we will address these questions, provide an overview of other diseases in which these antibodies are prevalent, and describe the physiological role of RhoGDI2 itself. If the mechanism and impact of RhoGDI2 antibodies in kidney graft failure are known, improved risk stratification can be provided to decrease the rate of donor kidney graft failure.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
