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CD8(+) T cells
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Transporter associated with peptide processing
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The MHC-E peptide ligands for checkpoint CD94/NKG2A are governed by inflammatory signals, whereas LILRB1/2 receptors are peptide indifferent
Intertumoral differences dictate the outcome of TGF-β blockade on the efficacy of viro-immunotherapy
In vivo modelling of cutaneous T-cell lymphoma
A Single-Domain TCR-like Antibody Selective for the Qa-1(b)/Qdm Peptide Complex Enhances Tumoricidal Activity of NK Cells via Blocking the NKG2A Immune Checkpoint
Targeting pancreatic cancer by TAK-981
Targeting pancreatic cancer by TAK-981
Preinduced reovirus-specific T-cell immunity enhances the anticancer efficacy of reovirus therapy
NKG2A is a late immune checkpoint on CD8 T cells and marks repeated stimulation and cell division
Metabolic stress in cancer cells induces immune escape through a PI3K-dependent blockade of IFN gamma receptor signaling
CD3-Bispecific Antibody Therapy Turns Solid Tumors into Inflammatory Sites but Does Not Install Protective Memory
T cells specific for a TAP-independent self-peptide remain naive in tumor-bearing mice and are fully exploitable for therapy
A herpesvirus encoded Qa-1 mimic inhibits natural killer cell cytotoxicity through CD94/NKG2A receptor engagement
A herpesvirus encoded Qa-1 mimic inhibits natural killer cell cytotoxicity through CD94/NKG2A receptor engagement
High Fc gamma R Expression on Intratumoral Macrophages Enhances Tumor-Targeting Antibody Therapy
NKG2A Blockade Potentiates CD8 T Cell Immunity Induced by Cancer Vaccines
T cells engaging the conserved Mhc class ib Molecule Qa-1(b) with TaP-independent Peptides are semi-invariant lymphocytes
Vaccination with proline-substituted neoepitope Trh4 generates enhanced CTL responses against tumors
CD4(+) T Cell and NK Cell Interplay Key to Regression of MHC Class I-low Tumors upon TLR7/8 Agonist Therapy
TAP-independent self-peptides enhance T cell recognition of immune-escaped tumors
Involvement of several alternative antigen processing routes for the MHC-I presentation of TAP-independent peptides
Therapeutic Peptide Vaccine-Induced CD8 T Cells Strongly Modulate Intratumoral Macrophages Required for Tumor Regression
Dominant contribution of the proteasome and metalloproteinases to TAP-independent MHC-I peptide repertoire
Limited Density of an Antigen Presented by RMA-S Cells Requires B7-1/CD28 Signaling to Enhance T-Cell Immunity at the Effector Phase
Inhibition of CSF-1R Supports T-Cell Mediated Melanoma Therapy
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