1. B7-H3 expression in donor T cells and host cells negatively regulates acute graft-versus-host disease lethality.

    Blood 125(21):3335 (2015) PMID 25814530 PMCID PMC4440885

    Members of the B7 family have been shown to be important for regulating immune responses by providing either positive or negative costimulatory signals. The function of B7-H3 has been controversial. We show that B7-H3 is upregulated in graft-versus-host disease (GVHD) target organs, including th...
  2. Immune checkpoint targeting in cancer therapy: toward combination strategies with curative potential.

    Cell 161(2):205 (2015) PMID 25860605

    Research in two fronts has enabled the development of therapies that provide significant benefit to cancer patients. One area stems from a detailed knowledge of mutations that activate or inactivate signaling pathways that drive cancer development. This work triggered the development of targeted...
  3. The future of immune checkpoint therapy.

    Science 348(6230):56 (2015) PMID 25838373

    Immune checkpoint therapy, which targets regulatory pathways in T cells to enhance antitumor immune responses, has led to important clinical advances and provided a new weapon against cancer. This therapy has elicited durable clinical responses and, in a fraction of patients, long-term remission...
  4. Anticancer immunotherapy by CTLA-4 blockade: obligatory contribution of IL-2 receptors and negative prognostic impact of soluble CD25.

    Cell Research 25(3):399 (2015) PMID 25732764 PMCID PMC4349252

  5. Anticancer immunotherapy by CTLA-4 blockade: obligatory contribution of IL-2 receptors and negative prognostic impact of soluble CD25.

    Cell Research 25(3):399 (2015) PMID 25732764 PMCID PMC4349252

  6. Friends Not Foes: CTLA-4 Blockade and mTOR Inhibition Cooperate during CD8+ T Cell Priming To Promote Memory Formation and Metabolic Readiness.

    Journal of Immunology 194(5):2089 (2015) PMID 25624453

    During primary Ag encounter, T cells receive numerous positive and negative signals that control their proliferation, function, and differentiation, but how these signals are integrated to modulate T cell memory has not been fully characterized. In these studies, we demonstrate that combining se...
  7. Friends Not Foes: CTLA-4 Blockade and mTOR Inhibition Cooperate during CD8+ T Cell Priming To Promote Memory Formation and Metabolic Readiness.

    Journal of Immunology 194(5):2089 (2015) PMID 25624453

    During primary Ag encounter, T cells receive numerous positive and negative signals that control their proliferation, function, and differentiation, but how these signals are integrated to modulate T cell memory has not been fully characterized. In these studies, we demonstrate that combining se...
  8. Anticancer immunotherapy by CTLA-4 blockade: obligatory contribution of IL-2 receptors and negative prognostic impact of soluble CD25.

    Cell Research 25(2):208 (2015) PMID 25582080

    The cytotoxic T lymphocyte antigen-4 (CTLA-4)-blocking antibody ipilimumab induces immune-mediated long-term control of metastatic melanoma in a fraction of patients. Although ipilimumab undoubtedly exerts its therapeutic effects via immunostimulation, thus far clinically useful, immunologically...
  9. Anticancer immunotherapy by CTLA-4 blockade: obligatory contribution of IL-2 receptors and negative prognostic impact of soluble CD25.

    Cell Research 25(2):208 (2015) PMID 25582080

    The cytotoxic T lymphocyte antigen-4 (CTLA-4)-blocking antibody ipilimumab induces immune-mediated long-term control of metastatic melanoma in a fraction of patients. Although ipilimumab undoubtedly exerts its therapeutic effects via immunostimulation, thus far clinically useful, immunologically...
  10. Checkpoint blockade cancer immunotherapy targets tumour-specific mutant antigens.

    Nature 515(7528):577 (2014) PMID 25428507 PMCID PMC4279952

    The immune system influences the fate of developing cancers by not only functioning as a tumour promoter that facilitates cellular transformation, promotes tumour growth and sculpts tumour cell immunogenicity, but also as an extrinsic tumour suppressor that either destroys developing tumours or ...
  11. Checkpoint blockade cancer immunotherapy targets tumour-specific mutant antigens.

    Nature 515(7528):577 (2014) PMID 25428507

    The immune system influences the fate of developing cancers by not only functioning as a tumour promoter that facilitates cellular transformation, promotes tumour growth and sculpts tumour cell immunogenicity, but also as an extrinsic tumour suppressor that either destroys developing tumours or ...
  12. Checkpoint blockade cancer immunotherapy targets tumour-specific mutant antigens.

    Nature 515(7528):577 (2014) PMID 25428507 PMCID PMC4279952

    The immune system influences the fate of developing cancers by not only functioning as a tumour promoter that facilitates cellular transformation, promotes tumour growth and sculpts tumour cell immunogenicity, but also as an extrinsic tumour suppressor that either destroys developing tumours or ...
  13. Checkpoint blockade cancer immunotherapy targets tumour-specific mutant antigens.

    Nature 515(7528):577 (2014) PMID 25428507 PMCID PMC4279952

    The immune system influences the fate of developing cancers by not only functioning as a tumour promoter that facilitates cellular transformation, promotes tumour growth and sculpts tumour cell immunogenicity, but also as an extrinsic tumour suppressor that either destroys developing tumours or ...
  14. Checkpoint blockade cancer immunotherapy targets tumour-specific mutant antigens.

    Nature 515(7528):577 (2014) PMID 25428507

    The immune system influences the fate of developing cancers by not only functioning as a tumour promoter that facilitates cellular transformation, promotes tumour growth and sculpts tumour cell immunogenicity, but also as an extrinsic tumour suppressor that either destroys developing tumours or ...
  15. Checkpoint blockade cancer immunotherapy targets tumour-specific mutant antigens.

    Nature 515(7528):577 (2014) PMID 25428507 PMCID PMC4279952

    The immune system influences the fate of developing cancers by not only functioning as a tumour promoter that facilitates cellular transformation, promotes tumour growth and sculpts tumour cell immunogenicity, but also as an extrinsic tumour suppressor that either destroys developing tumours or ...
  16. Cytotoxic T lymphocyte antigen-4 blockade enhances antitumor immunity by stimulating melanoma-specific T-cell motility.

    Cancer Immunology Research 2(10):970 (2014) PMID 25038199

    It is now clear that anti-CTLA-4 (α-CTLA-4) antibodies stimulate tumor immunity either by relieving inhibition of effector T-cell function or by depletion of regulatory T cells (Treg). Several recent reports, however, have suggested that these antibodies may deliver a "go" signal to effector T c...
  17. Cytotoxic T lymphocyte antigen-4 blockade enhances antitumor immunity by stimulating melanoma-specific T-cell motility.

    Cancer Immunology Research 2(10):970 (2014) PMID 25038199

    It is now clear that anti-CTLA-4 (α-CTLA-4) antibodies stimulate tumor immunity either by relieving inhibition of effector T-cell function or by depletion of regulatory T cells (Treg). Several recent reports, however, have suggested that these antibodies may deliver a "go" signal to effector T c...
  18. Combining radiation and immunotherapy: a new systemic therapy for solid tumors?

    Cancer Immunology Research 2(9):831 (2014) PMID 25187273

    With the recent success of checkpoint inhibitors and other immunomodulating agents, there has been renewed interest in the combination of such agents with radiation. The biologic premise behind such a strategy is that the tumor-antigen release achieved by localized radiation will promote specifi...
  19. Combining radiation and immunotherapy: a new systemic therapy for solid tumors?

    Cancer Immunology Research 2(9):831 (2014) PMID 25187273

    With the recent success of checkpoint inhibitors and other immunomodulating agents, there has been renewed interest in the combination of such agents with radiation. The biologic premise behind such a strategy is that the tumor-antigen release achieved by localized radiation will promote specifi...
  20. Depletion of carcinoma-associated fibroblasts and fibrosis induces immunosuppression and accelerates pancreas cancer with reduced survival.

    Cancer Cell 25(6):719 (2014) PMID 24856586 PMCID PMC4180632

    Pancreatic ductal adenocarcinoma (PDAC) is associated with marked fibrosis and stromal myofibroblasts, but their functional contribution remains unknown. Transgenic mice with the ability to delete αSMA(+) myofibroblasts in pancreatic cancer were generated. Depletion starting at either noninvasiv...