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1. Full Text TIGIT and PD-1 impair tumor antigen-specific CD8 + T cells in melanoma patients
by Chauvin, Joe-Marc and Pagliano, Ornella and Fourcade, Julien and Sun, Zhaojun and Wang, Hong and Sander, Cindy and Kirkwood, John M and Chen, Tseng-Hui Timothy and Maurer, Mark and Korman, Alan J and Zarour, Hassane M
Journal of Clinical Investigation, ISSN 0021-9738, 05/2015, Volume 125, Issue 5, pp. 2046 - 2058
T cell Ig and ITIM domain (TIGIT) is an inhibitory receptor expressed by activated T cells, Tregs, and NI( cells. Here, we determined that TIGIT is upregulated... 
MEDICINE, RESEARCH & EXPERIMENTAL | ADHESION MOLECULE | LIGANDS | DNAM-1 | INHIBITORY RECEPTORS | CHRONIC VIRAL-INFECTION | NECTIN-2 CD112 | UP-REGULATION | PVR CD155 | EXPRESSION | POLIOVIRUS RECEPTOR CD155 | Up-Regulation | Receptors, Immunologic - physiology | Receptors, Virus - biosynthesis | Humans | Neoplasm Proteins - physiology | Gene Expression Regulation, Neoplastic | Neoplasm Proteins - antagonists & inhibitors | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Programmed Cell Death 1 Receptor - physiology | Receptors, Virus - genetics | Receptors, Immunologic - antagonists & inhibitors | Receptors, Immunologic - biosynthesis | Programmed Cell Death 1 Receptor - biosynthesis | CD8-Positive T-Lymphocytes - metabolism | Lymphocytes, Tumor-Infiltrating - metabolism | Interleukin-2 Receptor beta Subunit - genetics | Neoplasm Proteins - genetics | Antibodies, Monoclonal - immunology | Antigen-Presenting Cells - metabolism | Antigens, Neoplasm - immunology | Lymphocyte Activation | Neoplasm Proteins - biosynthesis | Antibodies, Monoclonal - pharmacology | Immunophenotyping | Interleukin-2 Receptor beta Subunit - biosynthesis | Melanoma - pathology | Antigen-Presenting Cells - immunology | Melanoma - immunology | Antigens, Differentiation, T-Lymphocyte - genetics | Cell Line, Tumor | T-Cell Antigen Receptor Specificity | Immunologic Memory | Antigens, Differentiation, T-Lymphocyte - biosynthesis | CD8-Positive T-Lymphocytes - immunology | Receptors, Immunologic - genetics | Programmed Cell Death 1 Receptor - genetics | Cytokines - biosynthesis | Lymphocytes, Tumor-Infiltrating - immunology | Oncology | Immunology | Dermatology | Therapeutics
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2. Full Text Immune Checkpoint Blockade: A Common Denominator Approach to Cancer Therapy
by Topalian, Suzanne L and Drake, Charles G and Pardoll, Drew M
Cancer Cell, ISSN 1535-6108, 04/2015, Volume 27, Issue 4, pp. 450 - 461
The immune system recognizes and is poised to eliminate cancer but is held in check by inhibitory receptors and ligands. These immune checkpoint pathways,... 
METASTATIC MELANOMA | CTLA-4 BLOCKADE | SOLID TUMORS | ONCOLOGY | T-CELL-ACTIVATION | EFFECTOR FUNCTION | DOUBLE-BLIND | COSTIMULATORY MOLECULE | ANTITUMOR IMMUNITY | RESISTANT PROSTATE-CANCER | CHRONIC VIRAL-INFECTION | CELL BIOLOGY | CD28 Antigens - physiology | Antibodies, Monoclonal - pharmacology | Humans | Antibodies, Monoclonal - therapeutic use | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Antineoplastic Agents - therapeutic use | CD28 Antigens - immunology | Programmed Cell Death 1 Receptor - physiology | CTLA-4 Antigen - immunology | Models, Immunological | Neoplasms - immunology | Immunotherapy | CD28 Antigens - antagonists & inhibitors | Antineoplastic Agents - pharmacology | Programmed Cell Death 1 Receptor - immunology | CTLA-4 Antigen - antagonists & inhibitors | CTLA-4 Antigen - physiology | Antimitotic agents | Care and treatment | Antineoplastic agents | Health aspects | Cancer
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3. Full Text Immune inhibitory molecules LAG-3 and PD-1 synergistically regulate T-cell function to promote tumoral immune escape
by Woo, Seng-Ryong and Turnis, Meghan E and Goldberg, Monica V and Bankoti, Jaishree and Selby, Mark and Nirschl, Christopher J and Bettini, Matthew L and Gravano, David M and Vogel, Peter and Liu, Chih Long and Tangsombatvisit, Stephanie and Grosso, Joseph F and Netto, George and Smeltzer, Matthew P and Chaux, Alcides and Utz, Paul J and Workman, Creg J and Pardoll, Drew M and Korman, Alan J and Drake, Charles G and Vignali, Dario A. A
Cancer Research, ISSN 0008-5472, 02/2012, Volume 72, Issue 4, pp. 917 - 927
Inhibitory receptors on immune cells are pivotal regulators of immune escape in cancer. Among these inhibitory receptors, CTLA-4 (targeted clinically by... 
ACTIVATION | THERAPY | ONCOLOGY | IMMUNOTHERAPY | TOLERANCE | DEFICIENT | MICE | INDUCTION | RECEPTORS | CANCER | CUTTING EDGE | Antibodies - therapeutic use | Antigens, CD - immunology | Neoplasm Transplantation | Mice, Inbred C57BL | Neoplasms, Experimental - therapy | Programmed Cell Death 1 Receptor - physiology | CD4-Positive T-Lymphocytes - immunology | Drug Synergism | Neoplasms, Experimental - pathology | Animals | Immune Tolerance - immunology | Neoplasms, Experimental - immunology | Cell Line, Tumor | Antigens, CD - physiology | Mice | Programmed Cell Death 1 Receptor - immunology | Tumor Escape - immunology | T cells | LAG-3 | PD-1 | tumor | immunotherapy
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4. Full Text The Inhibitory Receptor PD-1 Regulates IgA Selection and Bacterial Composition in the Gut
by Shimpei Kawamoto and Thinh H. Tran and Mikako Maruya and Keiichiro Suzuki and Yasuko Doi and Yumi Tsutsui and Lucia M. Kato and Sidonia Fagarasan
Science, ISSN 0036-8075, 4/2012, Volume 336, Issue 6080, pp. 485 - 489
Immunoglobulin A (IgA) is essential to maintain the symbiotic balance between gut bacterial communities and the host immune system. Here we provide evidence... 
T lymphocytes | Receptors | Statistical analysis | Cytokines | B lymphocytes | REPORTS | Plasma cells | Bacteria | Mice | Small intestine | Genetic mutation | AFFINITY | MULTIDISCIPLINARY SCIENCES | MUTATION | DYNAMICS | GERMINAL CENTER | GENERATION | MICE | HYPERMUTATION | HELPER T-CELLS | Immunoglobulin A - biosynthesis | Germinal Center - immunology | Adoptive Transfer | Programmed Cell Death 1 Receptor - physiology | Plasma Cells - physiology | Genes, Immunoglobulin Heavy Chain | Feces - microbiology | Bacteria - immunology | Intestinal Mucosa - immunology | T-Lymphocytes, Helper-Inducer - immunology | Germinal Center - cytology | Intestine, Small - immunology | Symbiosis | Intestine, Small - microbiology | Bacterial Physiological Phenomena | Bacterial Load | Peyer's Patches - cytology | Animals | B-Lymphocytes - immunology | Immunoglobulin A - immunology | Lymphocyte Count | Peyer's Patches - immunology | Programmed Cell Death 1 Receptor - genetics | Plasma Cells - immunology | Physiological aspects | Research | Immunoglobulin A | Cell death | Health aspects | Microbial colonies | Immunoglobulins | Digestive system | Apoptosis | Immune system | Immune systems | Alterations | Deletion | Evolution | Palladium | Inhabitants
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5. Full Text PD-1 blockade enhances T-cell migration to tumors by elevating IFN-γ inducible chemokines
by Peng, Weiyi and Liu, Chengwen and Xu, Chunyu and Lou, Yanyan and Chen, Jieqing and Yang, Yan and Yagita, Hideo and Overwijk, Willem W and Lizeé, Gregory and Radvanyi, Laszlo and Hwu, Patrick
Cancer Research, ISSN 0008-5472, 10/2012, Volume 72, Issue 20, pp. 5209 - 5218
Adoptive cell transfer (ACT) is considered a promising modality for cancer treatment, but despite ongoing improvements, many patients do not experience... 
METASTATIC MELANOMA | ONCOLOGY | ANTITUMOR IMMUNE-RESPONSES | DEATH-1 PATHWAY | INFILTRATING LYMPHOCYTES | LENTIVECTOR IMMUNIZATION | MECHANISMS | UP-REGULATION | PHASE-I | EXPRESSION | CARCINOMA | Lymphocytes, Tumor-Infiltrating - cytology | Up-Regulation | Chemokines - biosynthesis | Cell Proliferation | Interferon-gamma - physiology | Mice, Transgenic | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Adoptive Transfer | Programmed Cell Death 1 Receptor - physiology | Neoplasms, Experimental - pathology | Animals | T-Lymphocytes - cytology | Mice | Neoplasms, Experimental - metabolism | Cell Movement | Adoptive cell transfer (ACT) | PD-1 | T cell-mediated antitumor immune response | melanoma immunotherapy
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6. Full Text Programmed death 1 protects from fatal circulatory failure during systemic virus infection of mice
by Frebel, Helge and Nindl, Veronika and Schuepbach, Reto A and Braunschweiler, Thomas and Richter, Kirsten and Vogel, Johannes and Wagner, Carsten A and Loffing-Cueni, Dominique and Kurrer, Michael and Ludewig, Burkhard and Oxenius, Annette
Journal of Experimental Medicine, ISSN 0022-1007, 12/2012, Volume 209, Issue 13, pp. 2485 - 2499
The inhibitory programmed death 1 (PD-1)-programmed death ligand 1 (PD-L1) pathway contributes to the functional down-regulation of T cell responses during... 
MEDICINE, RESEARCH & EXPERIMENTAL | RECEPTOR ALPHA-DYSTROGLYCAN | NITRIC-OXIDE SYNTHASE | PD-L1 EXPRESSION | ENDOTHELIAL-CELLS | MEDIATED INJURY | LASSA FEVER | DEFICIENT MICE | IMMUNOLOGY | CHRONIC VIRAL-INFECTION | T-CELL EXHAUSTION | LYMPHOCYTIC CHORIOMENINGITIS | Capillary Permeability - physiology | Pore Forming Cytotoxic Proteins - genetics | B7-H1 Antigen - deficiency | Histocompatibility Antigen H-2D | Programmed Cell Death 1 Receptor - physiology | Shock - prevention & control | Lymphocytic Choriomeningitis - immunology | Pulmonary Edema - etiology | Pulmonary Edema - physiopathology | H-2 Antigens - genetics | Hypotension - physiopathology | Lymphocytic Choriomeningitis - physiopathology | Pore Forming Cytotoxic Proteins - physiology | Hypotension - etiology | H-2 Antigens - physiology | Disease Models, Animal | Programmed Cell Death 1 Receptor - deficiency | Shock - immunology | B7-H1 Antigen - physiology | Signal Transduction | Lymphocytic Choriomeningitis - pathology | Mice, Inbred C57BL | Shock - physiopathology | Mice, Transgenic | Pore Forming Cytotoxic Proteins - deficiency | B7-H1 Antigen - genetics | Mice, Knockout | Animals | Endothelium, Vascular - pathology | Mice | CD8-Positive T-Lymphocytes - immunology | Programmed Cell Death 1 Receptor - genetics
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7. Full Text PD-L1 on tumor cells is sufficient for immune evasion in immunogenic tumors and inhibits CD8 T cell cytotoxicity
by Juneja, Vikram R and McGuire, Kathleen A and Manguso, Robert T and LaFleur, Martin W and Collins, Natalie and Nicholas Haining, W and Freeman, Gordon J and Sharpe, Arlene H
Journal of Experimental Medicine, ISSN 0022-1007, 04/2017, Volume 214, Issue 4, pp. 895 - 904
It is unclear whether PD-L1 on tumor cells is sufficient for tumor immune evasion or simply correlates with an inflamed tumor microenvironment. We used three... 
MEDICINE, RESEARCH & EXPERIMENTAL | ACTIVATION | MELANOMA | RECEPTOR | B7-H1 | CANCER-IMMUNOTHERAPY | IMMUNOLOGY | MYELOID CELLS | COMBINATION | EXPRESSION | CHECKPOINT BLOCKADE | ANTIGEN | B7-H1 Antigen - physiology | Tumor Escape | Lymphocyte Activation | Mice, Inbred C57BL | Tumor Microenvironment | Programmed Cell Death 1 Receptor - physiology | Animals | Colorectal Neoplasms - immunology | Melanoma - immunology | Cell Line, Tumor | Mice | CD8-Positive T-Lymphocytes - immunology | Cytotoxicity, Immunologic | Adenocarcinoma | Animal models | PD-1 protein | Toxicity | Tumor cells | CD8 antigen | Melanoma | Cytotoxicity | Inflammation | Lymphocytes T | Immunity | Anticancer properties | Immunosuppression | Clonal deletion | Immunogenicity | Lymphocytes | PD-L1 protein | Deletion | Antitumor activity | Biocompatibility | Genetic engineering | Inhibition | Tumors | 314
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8. Full Text Frontline Science: Defects in immune function in patients with sepsis are associated with PD‐1 or PD‐L1 expression and can be restored by antibodies targeting PD‐1 or PD‐L1
by Patera, Andriani C and Drewry, Anne M and Chang, Katherine and Beiter, Evan R and Osborne, Dale and Hotchkiss, Richard S
Journal of Leukocyte Biology, ISSN 0741-5400, 12/2016, Volume 100, Issue 6, pp. 1239 - 1254
Defective neutrophil and monocyte function in septic patients correlates with PD‐1 and PD‐L1 expression, and can be restored by antibodies targeting PD‐1 and... 
monocytes | immunosuppression | programmed cell death | neutrophils | Immunosuppression | Monocytes | Programmed cell death | Neutrophils | ACUTE LUNG INJURY | MULTIPLE ORGAN FAILURE | IMMUNOLOGY | T-CELL EXHAUSTION | CELL BIOLOGY | SYSTEMIC INFLAMMATION | TUMOR-NECROSIS-FACTOR | SEPTIC SHOCK PATIENTS | SCAVENGER RECEPTOR | INDUCED IMMUNOSUPPRESSION | SUPPRESSOR-CELLS | MURINE POLYMICROBIAL SEPSIS | HEMATOLOGY | Prospective Studies | Humans | Middle Aged | Critical Illness | Male | Monocytes - metabolism | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Monocytes - immunology | Programmed Cell Death 1 Receptor - physiology | CD8-Positive T-Lymphocytes - metabolism | Killer Cells, Natural - immunology | Adult | Female | Neutrophils - metabolism | B7-H1 Antigen - physiology | Sepsis - immunology | Lymphocyte Activation | Antibodies, Monoclonal - pharmacology | Neutrophils - immunology | Immunophenotyping | B7-H1 Antigen - immunology | B7-H1 Antigen - antagonists & inhibitors | Lipopolysaccharides - pharmacology | Killer Cells, Natural - metabolism | Programmed Cell Death 1 Receptor - immunology | CD8-Positive T-Lymphocytes - immunology | Tumor Necrosis Factor-alpha - biosynthesis | Phagocytosis | Spotlight on Leading Edge Research
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9. Full Text A threshold level of intratumor CD8+ T-cell PD1 expression dictates therapeutic response to anti-PD1
by Ngiow, Shin Foong and Young, Arabella and Jacquelot, Nicolas and Yamazaki, Takahiro and Enot, David and Zitvogel, Laurence and Smyth, Mark J
Cancer Research, ISSN 0008-5472, 09/2015, Volume 75, Issue 18, pp. 3800 - 3811
Despite successes, thus far, a significant proportion of the patients treated with anti-PD1 antibodies have failed to respond. We use mouse tumor models of... 
MELANOMA | FC-GAMMA-RIII | ONCOLOGY | PD-1 BLOCKADE | REJECTION | INCREASES | ANTIBODY | REGULATORY T | NIVOLUMAB | CHECKPOINTS | MPDL3280A | Mammary Neoplasms, Experimental - immunology | Neoplasm Proteins - physiology | Antibodies, Monoclonal - therapeutic use | Programmed Cell Death 1 Receptor - physiology | T-Lymphocytes, Regulatory - immunology | Colonic Neoplasms - immunology | Myeloid Cells - immunology | Programmed Cell Death 1 Receptor - biosynthesis | CD8-Positive T-Lymphocytes - metabolism | Female | Lymphocytes, Tumor-Infiltrating - metabolism | Neoplasm Proteins - genetics | Adaptive Immunity | Colonic Neoplasms - therapy | B7-H1 Antigen - physiology | Neoplasm Proteins - biosynthesis | Adenocarcinoma - immunology | Down-Regulation | Mice, Inbred C57BL | Gene Expression Regulation, Neoplastic - immunology | Mice, Transgenic | Mammary Neoplasms, Experimental - therapy | Tumor Microenvironment - immunology | Animals | Adenocarcinoma - therapy | Immunization, Passive | Myeloid Cells - metabolism | Mice | Mice, Inbred BALB C | CD8-Positive T-Lymphocytes - immunology | Programmed Cell Death 1 Receptor - genetics | Lymphocytes, Tumor-Infiltrating - immunology
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10. Full Text Strength of PD-1 signaling differentially affects T-cell effector functions
by Fang Wei and Shi Zhong and Zhengyu Ma and Hong Kong and Andrew Medvec and Rafi Ahmed and Gordon J. Freeman and Michelle Krogsgaard and James L. Riley
Proceedings of the National Academy of Sciences, ISSN 0027-8424, 07/2013, Volume 110, Issue 27, pp. E2480 - E2489
High surface expression of programmed death 1 (PD-1) is associated with T-cell exhaustion; however, the relationship between PD-1 expression and T-cell... 
TCR signaling | Peptide counting | HIV-1 specific T cell response | ACTIVATION | PROGRAMMED DEATH-1 | MULTIDISCIPLINARY SCIENCES | IN-VITRO | peptide counting | INFECTION | VIRAL PERSISTENCE | BLOCKADE | UP-REGULATION | EXPRESSION | EXHAUSTION | ANTIGEN | Interleukin-2 - metabolism | Tumor Necrosis Factor-alpha - metabolism | Chemokine CCL4 - biosynthesis | Programmed Cell Death 1 Receptor - chemistry | Receptors, Antigen, T-Cell, alpha-beta - physiology | Humans | Cells, Cultured | Programmed Cell Death 1 Receptor - physiology | Signal Transduction - immunology | HIV-1 - immunology | Models, Immunological | T-Lymphocytes - cytology | T-Lymphocytes - metabolism | Calcium Signaling - immunology | T-Lymphocytes - immunology | Receptors, Antigen, T-Cell, alpha-beta - metabolism | Interferon-gamma - biosynthesis | Cytotoxicity, Immunologic | Biological Sciences | PNAS Plus
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11. Full Text Blockade of the PD-1/PD-L1 axis augments lysis of AML cells by the CD33/CD3 BiTE antibody construct AMG 330: Reversing a T-cell-induced immune escape mechanism
by Krupka, C and Kufer, P and Kischel, R and Zugmaier, G and Lichtenegger, F.S and Köhnke, T and Vick, B and Jeremias, I and Metzeler, K.H and Altmann, T and Schneider, S and Fiegl, M and Spiekermann, K and Bauerle, P.A and Hiddemann, W and Riethmüller, G and Subklewe, M
Leukemia, ISSN 0887-6924, 02/2016, Volume 30, Issue 2, pp. 484 - 491
Bispecific T-cell engagers (BiTEs) are very effective in recruiting and activating T cells. We tested the cytotoxicity of the CD33/CD3 BITE antibody construct... 
STIMULATION | LIGANDS | ONCOLOGY | IMMUNOTHERAPY | SINGLE-CHAIN ANTIBODY | TARGETS | ENGAGING ANTIBODY | ACUTE MYELOID-LEUKEMIA | HEMATOLOGY | HEMATOLOGIC MALIGNANCIES | CANCER | EXPRESSION | Tumor Escape - drug effects | B7-H1 Antigen - physiology | Antibodies, Bispecific - pharmacology | Leukemia, Myeloid, Acute - pathology | Sialic Acid Binding Ig-like Lectin 3 - analysis | Humans | Programmed Cell Death 1 Receptor - analysis | Programmed Cell Death 1 Receptor - antagonists & inhibitors | Leukemia, Myeloid, Acute - immunology | Programmed Cell Death 1 Receptor - physiology | Animals | B7-H1 Antigen - antagonists & inhibitors | Leukemia, Myeloid, Acute - drug therapy | T-Lymphocytes - immunology | B7-H1 Antigen - analysis | Mice | Genetic aspects | Regulation | Immune response | T cells | Health aspects
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