Antibody-mediated rejection (ABMR) remains one of the most challenging issues after organ transplantation and particularly after kidney transplantation. Despite many progresses during the last decade, ABMR is still the main cause of kidney graft loss and this all over the post- transplant period.

In this review, we describe the recent knowledge about molecular and cellular mechanisms involved in ABMR. We focused our report on the role of the complement pathway in the process of ABMR and we give some insights into the role of inflammatory cells, NK lymphocytes and the role of endothelial cells. We further describe the potential role of non-HLA antibodies, of which the importance has been increasingly emphasized in recent years.

Overall, this report could be of interest for all physicians who are working in the field of organ transplantation or who are working in the field of immunology. It gives essential information to understand new diagnosis advances and further therapeutic approaches.

Antibody-mediated rejection (ABMR) is the leading cause of graft failure ([1Sellares J., de Freitas D.G., Mengel M., Reeve J., Einecke G., Sis B., y al. Understanding the causes of kidney transplant failure: the dominant role of antibody-mediated rejection and nonadherence Am J Transplant 2012 ;  12 (2) : 388-399 [cross-ref]

Haga clic aquí para ir a la sección de Referencias,2El-Zoghby Z.M., Stegall M.D., Lager D.J., Kremers W.K., Amer H., Gloor J.M., y al. Identifying Specific Causes of Kidney Allograft Loss Am J Transplant 2009 ;  9 (3) : 527-535 [cross-ref]

Haga clic aquí para ir a la sección de Referencias]). In contrast to T-cell mediated rejection usually sensitive to steroids, active ABMR remains a therapeutic challenge. ABMR diagnosis relies on the presence of renal injuries and donor-specific antibodies (DSA) (HLA and non HLA antibodies) with sometimes the evidence of interaction between DSA and graft endothelium. Regularly revised during expert conferences, ABMR definition is currently categorized as active or chronic active. [3Haas M., Loupy A., Lefaucheur C., Roufosse C., Glotz D., Seron D., y al. The Banff 2017 Kidney Meeting Report: revised diagnostic criteria for chronic active T cell-mediated rejection, antibody-mediated rejection, and prospects for integrative endpoints for next-generation clinical trials Am J Transplant 2018 ;  18 (2) : 293-307 [cross-ref]

Haga clic aquí para ir a la sección de Referencias] The emergence of validated molecular assays targeting a better phenotyping of ABMR and the recent advances regarding the detrimental effect of DSA directed against minor antigens open the way to a better assessment of the heterogeneity of ABMR. In this review, we will address new aspects of ABMR regarding its mechanisms, diagnosis and treatments.