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PD-1-expressing tumor-infiltrating T cells are a favorable prognostic biomarker in HPV-associated head and neck cancer.
These findings prompt a need to revisit the significance of PD-1-infiltrating T cells in cancer, where it is suggested thatPD-1 detection may reflect a previous immune response against tumors that might be reactivated by PD- 1/PD-L1 blockade.
Regulatory T cells recruited through CCL22/CCR4 are selectively activated in lymphoid infiltrates surrounding primary breast tumors and lead to an adverse clinical outcome.
Results show that Treg are selectively recruited within lymphoid infiltrates and activated by mature DC likely through TAA presentation, resulting in the prevention of effector T-cell activation, immune escape, and ultimately tumor progression.
Human breast cancer cells enhance self tolerance by promoting evasion from NK cell antitumor immunity.
The data show that breast tumor progression involves NK cell dysfunction and that breast tumors model their environment to evade NK cell antitumor immunity, highlighting the importance of developing future therapies able to restore NK cell cytotoxicity to limit/prevent tumor escape from antitUMor immunity.
CD8(+) T cells specific for tumor antigens can be rendered dysfunctional by the tumor microenvironment through upregulation of the inhibitory receptors BTLA and PD-1.
These findings indicate that targeting BTLA along with the PD-1 and Tim-3 pathways is critical to reverse an important mechanism of immune escape in patients with advanced melanoma.
Key implication of CD277/butyrophilin-3 (BTN3A) in cellular stress sensing by a major human γδ T-cell subset.
A novel role played by B7-like molecules in human γδ T-cell antigenic activation is demonstrated and paves the way for new strategies to improve the efficiency of immunotherapies using Vγ9Vδ2 T cells.
PD-L1 and PD-L2 differ in their molecular mechanisms of interaction with PD-1.
The molecular mechanisms of PD-1 interactions with its ligands by surface plasmon resonance and cell surface binding as well as the ability of the two ligands to compete forPD-1 binding are investigated to suggest possible new approach for the therapy of chronic infection, cancer and transplantation.
CpG methylation controls reactivation of HIV from latency
Background DNA methylation of retroviral promoter and enhancer localized in the provirus 5’ long terminal repeat (LTR) is considered to be a mechanism of transcriptional suppression that allows
Raft nanodomains contribute to Akt/PKB plasma membrane recruitment and activation.
It is reported here that highly dynamic nanodomains exist in both the outer and inner leaflets of the plasma membrane and it is demonstrated that rafts are critically involved in the activation of a signaling axis that is essential for cell physiology.
Binding of phosphatidylinositol-3-OH kinase to CD28 is required for T-cell signalling
In the Acknowledgements section of this letter, the financial support for R.R. was the recipient of an INSERM fellowship and is now supported by a centennial fellowship of the MRC of Canada.
BTLA mediates inhibition of human tumor-specific CD8+ T cells that can be partially reversed by vaccination.
It is demonstrated that as human viral antigen-specific CD8+ T cells differentiated from naive to effector cells, their surface expression of BTLA was gradually downregulated and addition of CpG oligodeoxynucleotides to the vaccine formulation led to progressive downregulation of BTla in vivo and consequent resistance to BTLA-HVEM-mediated inhibition.