1. Characterization of PD-L1 Expression and Associated T-cell Infiltrates in Metastatic Melanoma Samples from Variable Anatomic Sites.

    Clinical Cancer Research 21(13):3052 (2015) PMID 25788491 PMCID PMC4490112

    Programmed death ligand-1 (PD-L1) tumor expression represents a mechanism of immune escape for melanoma cells. Drugs blocking PD-L1 or its receptor have shown unprecedented activity in melanoma, and our purpose was to characterize tumor PD-L1 expression and associated T-cell infiltration in meta...
  2. Focusing and sustaining the antitumor CTL effector killer response by agonist anti-CD137 mAb.

    PNAS 112(24):7551 (2015) PMID 26034288 PMCID PMC4475992

    Cancer immunotherapy is undergoing significant progress due to recent clinical successes by refined adoptive T-cell transfer and immunostimulatory monoclonal Ab (mAbs). B16F10-derived OVA-expressing mouse melanomas resist curative immunotherapy with either adoptive transfer of activated anti-OVA...
  3. PD-1 Upregulated on Regulatory T Cells during Chronic Virus Infection Enhances the Suppression of CD8+ T Cell Immune Response via the Interaction with PD-L1 Expressed on CD8+ T Cells.

    Journal of Immunology 194(12):5801 (2015) PMID 25934860

    Regulatory T (Treg) cells act as terminators of T cell immuniy during acute phase of viral infection; however, their role and suppressive mechanism in chronic viral infection are not completely understood. In this study, we compared the phenotype and function of Treg cells during acute or chroni...
  4. Mechanistic Assessment of PD-1H Coinhibitory Receptor-Induced T Cell Tolerance to Allogeneic Antigens.

    Journal of Immunology 194(11):5294 (2015) PMID 25917101 PMCID PMC4433880

    PD-1H is a recently identified cell surface coinhibitory molecule of the B7/CD28 immune modulatory gene family. We showed previously that single injection of a PD-1H agonistic mAb protected mice from graft-versus-host disease (GVHD). In this study, we report two distinct mechanisms operate in PD...
  5. PD-1 Suppresses Protective Immunity to Streptococcus pneumoniae through a B Cell-Intrinsic Mechanism.

    Journal of Immunology 194(5):2289 (2015) PMID 25624454 PMCID PMC4339454

    Despite the emergence of the programmed cell death 1 (PD-1):PD-1 ligand (PD-L) regulatory axis as a promising target for treating multiple human diseases, remarkably little is known about how this pathway regulates responses to extracellular bacterial infections. We found that PD-1(-/-) mice, as...
  6. PD-1 Suppresses Protective Immunity to Streptococcus pneumoniae through a B Cell-Intrinsic Mechanism.

    Journal of Immunology 194(5):2289 (2015) PMID 25624454

    Despite the emergence of the programmed cell death 1 (PD-1):PD-1 ligand (PD-L) regulatory axis as a promising target for treating multiple human diseases, remarkably little is known about how this pathway regulates responses to extracellular bacterial infections. We found that PD-1(-/-) mice, as...
  7. PD-1 Suppresses Protective Immunity to Streptococcus pneumoniae through a B Cell-Intrinsic Mechanism.

    Journal of Immunology 194(5):2289 (2015) PMID 25624454

    Despite the emergence of the programmed cell death 1 (PD-1):PD-1 ligand (PD-L) regulatory axis as a promising target for treating multiple human diseases, remarkably little is known about how this pathway regulates responses to extracellular bacterial infections. We found that PD-1(-/-) mice, as...
  8. PD-1 suppresses protective immunity to Streptococcus pneumoniae through a B cell-intrinsic mechanism.

    Journal of Immunology 194(5):2289 (2015) PMID 25624454 PMCID PMC4339454

    Despite the emergence of the programmed cell death 1 (PD-1):PD-1 ligand (PD-L) regulatory axis as a promising target for treating multiple human diseases, remarkably little is known about how this pathway regulates responses to extracellular bacterial infections. We found that PD-1(-/-) mice, as...
  9. B7H1/CD80 interaction augments PD-1-dependent T cell apoptosis and ameliorates graft-versus-host disease.

    Journal of Immunology 194(2):560 (2015) PMID 25488990 PMCID PMC4282988

    Interactions of B7H1 (programmed death ligand 1 [PD-L1]) with its two ligands, PD-1 and CD80, on T cells play a pivotal role in controlling T cell activation, proliferation, anergy, and apoptosis. However, the interactions between the two pathways remain unknown. Using an alloimmune response mod...
  10. B7H1/CD80 interaction augments PD-1-dependent T cell apoptosis and ameliorates graft-versus-host disease.

    Journal of Immunology 194(2):560 (2015) PMID 25488990 PMCID PMC4282988

    Interactions of B7H1 (programmed death ligand 1 [PD-L1]) with its two ligands, PD-1 and CD80, on T cells play a pivotal role in controlling T cell activation, proliferation, anergy, and apoptosis. However, the interactions between the two pathways remain unknown. Using an alloimmune response mod...
  11. B7-H3 Promotes Pathogenesis of Autoimmune Disease and Inflammation by Regulating the Activity of Different T Cell Subsets.

    PLoS ONE 10(6):e0130126 (2015) PMID 26065426 PMCID PMC4465912

    B7-H3 is a cell surface molecule in the immunoglobulin superfamily that is frequently upregulated in response to autoantigens and pathogens during host T cell immune responses. However, B7-H3's role in the differential regulation of T cell subsets remains largely unknown. Therefore, we construct...
  12. Intermittent chemotherapy can retain the therapeutic potential of anti-CD137 antibody during the late tumor-bearing state.

    Cancer Science 106(1):9 (2015) PMID 25363339

    Immunomodulating monoclonal antibodies (mAb) can evoke antitumor T-cell responses, which are attenuated by regulatory T cells (Treg) and myeloid-derived suppressor cells (MDSC). Treatment with cyclophosphamide (CP) and gemcitabine (GEM) can mitigate the immunosuppression by Treg and MDSC, respec...
  13. Intermittent chemotherapy can retain the therapeutic potential of anti-CD137 antibody during the late tumor-bearing state.

    Cancer Science 106(1):9 (2015) PMID 25363339

    Immunomodulating monoclonal antibodies (mAb) can evoke antitumor T-cell responses, which are attenuated by regulatory T cells (Treg) and myeloid-derived suppressor cells (MDSC). Treatment with cyclophosphamide (CP) and gemcitabine (GEM) can mitigate the immunosuppression by Treg and MDSC, respec...
  14. Myeloid cells' evasion of melanoma immunity.

    Journal of Investigative Dermatology 134(11):2675 (2014) PMID 25318429

    An immune-suppressive role of myeloid-derived suppressor cells (MDSCs) in melanoma has long been speculated, whereas molecular mechanisms underlying this role are not well understood. Here, Chung and colleagues show that dendritic cell-associated, heparan sulfate proteoglycans-dependent integrin...
  15. Myeloid cells' evasion of melanoma immunity.

    Journal of Investigative Dermatology 134(11):2675 (2014) PMID 25318429 PMCID PMC4455019

    An immune-suppressive role of myeloid-derived suppressor cells (MDSCs) in melanoma has long been speculated, whereas molecular mechanisms underlying this role are not well understood. Here, Chung and colleagues show that dendritic cell-associated, heparan sulfate proteoglycans-dependent integrin...
  16. Myeloid cells' evasion of melanoma immunity.

    Journal of Investigative Dermatology 134(11):2675 (2014) PMID 25318429

    An immune-suppressive role of myeloid-derived suppressor cells (MDSCs) in melanoma has long been speculated, whereas molecular mechanisms underlying this role are not well understood. Here, Chung and colleagues show that dendritic cell-associated, heparan sulfate proteoglycans-dependent integrin...
  17. Association of PD-1, PD-1 ligands, and other features of the tumor immune microenvironment with response to anti-PD-1 therapy.

    Clinical Cancer Research 20(19):5064 (2014) PMID 24714771 PMCID PMC4185001

    Immunomodulatory drugs differ in mechanism-of-action from directly cytotoxic cancer therapies. Identifying factors predicting clinical response could guide patient selection and therapeutic optimization. Patients (N = 41) with melanoma, non-small cell lung carcinoma (NSCLC), renal cell carcinoma...
  18. Association of PD-1, PD-1 ligands, and other features of the tumor immune microenvironment with response to anti-PD-1 therapy.

    Clinical Cancer Research 20(19):5064 (2014) PMID 24714771 PMCID PMC4185001

    Immunomodulatory drugs differ in mechanism-of-action from directly cytotoxic cancer therapies. Identifying factors predicting clinical response could guide patient selection and therapeutic optimization. Patients (N = 41) with melanoma, non-small cell lung carcinoma (NSCLC), renal cell carcinoma...
  19. Programmed death-1 pathway in host tissues ameliorates Th17/Th1-mediated experimental chronic graft-versus-host disease.

    Journal of Immunology 193(5):2565 (2014) PMID 25080485

    Chronic graft-versus-host disease (GVHD) is a major cause of late death and morbidity after allogeneic hematopoietic cell transplantation, but its pathogenesis remains unclear. We investigated the role of the programmed death-1 (PD-1) pathway in chronic GVHD using a well-defined mouse model of B...
  20. Programmed death-1 pathway in host tissues ameliorates Th17/Th1-mediated experimental chronic graft-versus-host disease.

    Journal of Immunology 193(5):2565 (2014) PMID 25080485

    Chronic graft-versus-host disease (GVHD) is a major cause of late death and morbidity after allogeneic hematopoietic cell transplantation, but its pathogenesis remains unclear. We investigated the role of the programmed death-1 (PD-1) pathway in chronic GVHD using a well-defined mouse model of B...