Evolving Therapeutic Approaches for Treatment of Antibody-Mediated Rejection in Renal Allograft Recipients

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Stanley C Jordan1, Noriko Ammerman2, Edmund Huang2

  • 1Comprehensive Transplant Center, Cedars-Sinai Medical Center, West Hollywood, CA, USA. stan.jordan@cshs.org.

Results and Problems in Cell Differentiation
|January 1, 2026
PubMed

Antibody-mediated rejection (AMR) is now recognized as the primary cause of the decline of functional integrity and ultimately, graft failure in kidney transplants. Evolving understanding of effectors responsible for B-cell activation and plasma cell biology has led to the informed design of new therapeutics. Currently, several novel agents with varying mechanisms of action have emerged. These include imlifidase, FcRn inhibitors, anti-cytokine (IL-6/IL-6R) therapies, and plasma cell-directed therapies, especially anti-CD38s. As our understanding of critical effector pathways responsible for ARM grows, we now know that no single agent can control all facets of antibody generation and injury. The future of antibody-directed therapeutics will require protocols consisting of multiple agents positioned in a logical sequence to rapidly and durably remove pathogenic DSAs and block their re-emergence.

Keywords:
Anti-CD20Anti-CD38Antibody-dependent cellular cytotoxicity (ADCC)Antibody-mediated rejectionB cellsComplement-dependent cytotoxicity (CDC)FcRn inhibitors anti-IL-6/IL-6RImlifidaseKidney transplantationPlasma cells

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