Eculizumab in renal transplantation
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Cited by (35)
Complement deficiencies
2020, Stiehm's Immune Deficiencies: Inborn Errors of ImmunityThe recipient of a renal transplant
2019, Kidney Transplantation - Principles and PracticeDe Novo and Recurrence of Renal Disease
2017, Kidney Transplantation, Bioengineering, and Regeneration: Kidney Transplantation in the Regenerative Medicine EraAntiphospholipid syndrome and kidney disease
2017, Kidney InternationalCitation Excerpt :Importantly, we observed that the preclusion of mTORC activation with sirolimus in APS transplant recipients was associated with a drastic reduction of vascular cell proliferation that correlated with a frank reduction in APSN renal lesions and preserved renal function.13 It is interesting to note that the recruitment of the AKT/mTORC pathway in endothelial cells is not triggered solely by APS but also was observed in many conditions associated with endothelium injuries, such as mechanical traumatisms or anti–human leukocyte antigen antibodies after organ transplantation.93–95 These data suggest that the AKT/mTORC pathway is a common final pathway for many endothelial injuries,93 representing, perhaps in some conditions, a potential therapeutic target.93,96–98
Transplantation Immunology: Kidney and Liver
2016, Encyclopedia of ImmunobiologyComplement in therapy and disease. Regulating the complement system with antibody-based therapeutics.
2015, Molecular ImmunologyCitation Excerpt :Both clinical and subclinical antibody-mediated rejection have been recognized as major causes of allograft loss (Amico et al., 2009), which is usually unresponsive to conventional anti-rejection therapy, such as suppression of the T-cell-dependent antibody response, removal of donor reactive antibodies, blocking residual allo-antibodies, and depletion of naive and memory B-cells. Convincing, but still limited, evidence has shown that eculizumab is efficient in preventing both acute and chronic antibody-mediated rejection and clinical studies further extending these results are ongoing (Legendre et al., 2013). Graft-versus-host disease (GvHD) is at the other side of the spectrum of clinical complications of allo-transplantation and is mediated by donor T-cells that attack host cells, leading to epithelial tissue injury in skin, intestine, and liver (Shlomchik, 2007).