Background: The inhibitory functions triggered by the programmed cell death-1 (PD-1) receptor following binding to its ligand (PD-L1) protect healthy organs from cytotoxic T cells, and neutralize antitumor T cell attack. Antibody-based therapies to block PD-1/PD-L1 interaction have yielded notable results, but most patients eventually develop resistance. This failure is attributed to CD8 T cells achieving hyporesponsive states from which recovery is hardly feasible.
View Article and Find Full Text PDFBackground: Preclinical research suggests that the efficacy of immune checkpoint inhibitors in breast cancer can be enhanced by combining them with antiangiogenics, particularly in a sequential fashion. We sought to explore the efficacy and biomarkers of combining the anti-PD-L1 durvalumab plus the antiangiogenic bevacizumab after bevacizumab monotherapy for advanced HER2-negative breast cancer.
Methods: Patients had advanced HER2-negative disease that progressed while receiving single-agent bevacizumab maintenance as a part of a previous chemotherapy plus bevacizumab regimen.
The chemokine receptor CCR6 is expressed by CD4+ T cell effector/memory and regulatory effector/memory (TREM) subsets. Here we show that CCR6 modulates graft-versus-host-disease (GVHD) responses in both alloreactive CD4+ T effector cells and regulatory T (Treg) cells. Mortality and morbidity due to acute GVHD were drastically reduced and delayed when naïve T cells were derived from CCR6-deficient donor mice.
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