Targeting tissue immune memory in chronic-remitting autoimmune kidney diseases: current concepts and future therapies

Immune-mediated kidney diseases have a substantial disease burden and frequent disease relapses significantly contribute to the high morbidity. Relapsing disease courses are associated with poor outcome and accelerated progression to end-stage renal disease. The pathomechanisms leading to relapse are diverse and only incompletely understood. Both adaptive and innate immune cells are implicated in the immune memory of these diseases. In addition to antigen-dependent mechanisms of T and B cells, persistent epigenetic and metabolic changes in adaptive and innate immune cells may sustain immunological memory and thereby provide a cellular and molecular basis for relapse. Treatment options, especially in frequently relapsing cases, are limited and memory immune cells often evade standard immunosuppressive therapies. As our understanding of immunological memory continues to improve, new treatment options emerge. Improved depletion of B cells, antigen-specific cell-based therapies and redirecting epigenetic alterations may target long-lasting immune memory. This could reduce relapse risk and improve long-term outcomes in patients with immune-mediated kidney diseases.