Immune checkpoint inhibitors (ICI) are a novel class of anticancer therapy that has revolutionized the treatment of different cancer types. They are humanized antibodies against target inhibitors receptors (CTLA-4, PD-1) and ligands (PD-1) expressed on T cells, peripheral tissue, and tumoral cells. They enhance the antitumoral response by unleashing the breaks on the immune system but can provoke uncontrolled off-target effects, the so-called immune-related adverse events. Nephrotoxicity is rare but may occur in up to 4% of the patients and the most frequent lesions seen on biopsy are interstitial nephritis and acute tubular necrosis.
A particularly relevant patients population that could benefit from ICI are kidney transplant recipients (KTR)s. The rejection rate has been reported to be as high as 42% in KTR and it is associated with an important rate of graft loss.
Acute interstitial nephritis (AIN) due to ICI is more frequently encountered than initially reported in early clinical trials. Only 40% of the patients recover completely after withdrawal of ICI and/or treatment with corticosteroids. Lack of recovery has been associated with increased mortality. In KTRs rejection rates are high and transplant outcomes are poor after rejection. Little is known on how to treat rejection in this patient population and how to diminish the risk of rejection before administering ICI. In the upcoming era of precision medicine, biomarkers associated with poor kidney outcomes need to be sought and would allow us to inform patients about their risk of graft loss or nephrotoxicity before the administration of ICI.
In this Research Topic, we aim to understand the pathological pathways leading to ICI-AIN and ICI-induced allograft rejection to better treat and prevent these adverse events.
We welcome the submission of original research articles, reviews, and mini-reviews covering but not limited to, the following sub-topics:
• Activation of immunosenescent antigen-specific cytotoxic T-cells after ICI
• Influence of tumor on host immune responses
• Effect of PD-1 and PD-L1 pathway blockage on Treg and other alloreactive or autoreactive T and B cells
• Non-invasive biomarkers of graft rejection and acute interstitial nephritis
• Role of PD-1 and PD-L1 expression on renal tubular cells in tissue protection
• Role of drug-specific T-cells in ICI induced acute interstitial nephritis
• Immune profiling after ICI
• Tumoral response after ICI in KTR
Immune checkpoint inhibitors (ICI) are a novel class of anticancer therapy that has revolutionized the treatment of different cancer types. They are humanized antibodies against target inhibitors receptors (CTLA-4, PD-1) and ligands (PD-1) expressed on T cells, peripheral tissue, and tumoral cells. They enhance the antitumoral response by unleashing the breaks on the immune system but can provoke uncontrolled off-target effects, the so-called immune-related adverse events. Nephrotoxicity is rare but may occur in up to 4% of the patients and the most frequent lesions seen on biopsy are interstitial nephritis and acute tubular necrosis.
A particularly relevant patients population that could benefit from ICI are kidney transplant recipients (KTR)s. The rejection rate has been reported to be as high as 42% in KTR and it is associated with an important rate of graft loss.
Acute interstitial nephritis (AIN) due to ICI is more frequently encountered than initially reported in early clinical trials. Only 40% of the patients recover completely after withdrawal of ICI and/or treatment with corticosteroids. Lack of recovery has been associated with increased mortality. In KTRs rejection rates are high and transplant outcomes are poor after rejection. Little is known on how to treat rejection in this patient population and how to diminish the risk of rejection before administering ICI. In the upcoming era of precision medicine, biomarkers associated with poor kidney outcomes need to be sought and would allow us to inform patients about their risk of graft loss or nephrotoxicity before the administration of ICI.
In this Research Topic, we aim to understand the pathological pathways leading to ICI-AIN and ICI-induced allograft rejection to better treat and prevent these adverse events.
We welcome the submission of original research articles, reviews, and mini-reviews covering but not limited to, the following sub-topics:
• Activation of immunosenescent antigen-specific cytotoxic T-cells after ICI
• Influence of tumor on host immune responses
• Effect of PD-1 and PD-L1 pathway blockage on Treg and other alloreactive or autoreactive T and B cells
• Non-invasive biomarkers of graft rejection and acute interstitial nephritis
• Role of PD-1 and PD-L1 expression on renal tubular cells in tissue protection
• Role of drug-specific T-cells in ICI induced acute interstitial nephritis
• Immune profiling after ICI
• Tumoral response after ICI in KTR