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  1. Article ; Online: Recent advancements in the B7/CD28 immune checkpoint families: new biology and clinical therapeutic strategies.

    Pulanco, Marc C / Madsen, Anne T / Tanwar, Ankit / Corrigan, Devin T / Zang, Xingxing

    Cellular & molecular immunology

    2023  Volume 20, Issue 7, Page(s) 694–713

    Abstract: The B7/CD28 families of immune checkpoints play vital roles in negatively or positively regulating immune cells in homeostasis and various diseases. Recent basic and clinical studies have revealed novel biology of the B7/CD28 families and new ... ...

    Abstract The B7/CD28 families of immune checkpoints play vital roles in negatively or positively regulating immune cells in homeostasis and various diseases. Recent basic and clinical studies have revealed novel biology of the B7/CD28 families and new therapeutics for cancer therapy. In this review, we discuss the newly discovered KIR3DL3/TMIGD2/HHLA2 pathways, PD-1/PD-L1 and B7-H3 as metabolic regulators, the glycobiology of PD-1/PD-L1, B7x (B7-H4) and B7-H3, and the recently characterized PD-L1/B7-1 cis-interaction. We also cover the tumor-intrinsic and -extrinsic resistance mechanisms to current anti-PD-1/PD-L1 and anti-CTLA-4 immunotherapies in clinical settings. Finally, we review new immunotherapies targeting B7-H3, B7x, PD-1/PD-L1, and CTLA-4 in current clinical trials.
    MeSH term(s) Humans ; CD28 Antigens/metabolism ; B7-H1 Antigen/metabolism ; Neoplasms/therapy ; Immunotherapy ; Biology ; Immunoglobulins/metabolism
    Chemical Substances CD28 Antigens ; B7-H1 Antigen ; HHLA2 protein, human ; Immunoglobulins
    Language English
    Publishing date 2023-04-17
    Publishing country China
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2435097-7
    ISSN 2042-0226 ; 1672-7681
    ISSN (online) 2042-0226
    ISSN 1672-7681
    DOI 10.1038/s41423-023-01019-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: The immune checkpoint B7x expands tumor-infiltrating Tregs and promotes resistance to anti-CTLA-4 therapy.

    John, Peter / Pulanco, Marc C / Galbo, Phillip M / Wei, Yao / Ohaegbulam, Kim C / Zheng, Deyou / Zang, Xingxing

    Nature communications

    2022  Volume 13, Issue 1, Page(s) 2506

    Abstract: Immune checkpoint molecules play critical roles in regulating the anti-tumor immune response, and tumor cells often exploit these pathways to inhibit and evade the immune system. The B7-family immune checkpoint B7x is widely expressed in a broad variety ... ...

    Abstract Immune checkpoint molecules play critical roles in regulating the anti-tumor immune response, and tumor cells often exploit these pathways to inhibit and evade the immune system. The B7-family immune checkpoint B7x is widely expressed in a broad variety of cancer types, and is generally associated with advanced disease progression and poorer clinical outcomes, but the underlying mechanisms are unclear. Here, we show that transduction and stable expression of B7x in multiple syngeneic tumor models leads to the expansion of immunosuppressive regulatory T cells (Tregs). Mechanistically, B7x does not cause increased proliferation of Tregs in tumors, but instead promotes the conversion of conventional CD4
    MeSH term(s) B7 Antigens/immunology ; Humans ; Immunotherapy ; Neoplasms/drug therapy ; Neoplasms/therapy ; T-Lymphocytes, Regulatory
    Chemical Substances B7 Antigens
    Language English
    Publishing date 2022-05-06
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-022-30143-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: PD-L1 and B7-1 Cis-Interaction: New Mechanisms in Immune Checkpoints and Immunotherapies.

    Nishimura, Christopher D / Pulanco, Marc C / Cui, Wei / Lu, Liming / Zang, Xingxing

    Trends in molecular medicine

    2020  Volume 27, Issue 3, Page(s) 207–219

    Abstract: Immune checkpoints negatively regulate immune cell responses. Programmed cell death protein 1:programmed death ligand 1 (PD-1:PD-L1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4):B7-1 are among the most important immune checkpoint pathways, ... ...

    Abstract Immune checkpoints negatively regulate immune cell responses. Programmed cell death protein 1:programmed death ligand 1 (PD-1:PD-L1) and cytotoxic T lymphocyte-associated protein 4 (CTLA-4):B7-1 are among the most important immune checkpoint pathways, and are key targets for immunotherapies that seek to modulate the balance between stimulatory and inhibitory signals to lead to favorable therapeutic outcomes. The current dogma of these two immune checkpoint pathways has regarded them as independent with no interactions. However, the newly characterized PD-L1:B7-1 ligand-ligand cis-interaction and its ability to bind CTLA-4 and CD28, but not PD-1, suggests that these pathways have significant crosstalk. Here, we propose that the PD-L1:B7-1 cis-interaction brings novel mechanistic understanding of these pathways, new insights into mechanisms of current immunotherapies, and fresh ideas to develop better treatments in a variety of therapeutic settings.
    MeSH term(s) Autoimmune Diseases/immunology ; Autoimmune Diseases/therapy ; B7-1 Antigen/chemistry ; B7-1 Antigen/immunology ; B7-H1 Antigen/chemistry ; B7-H1 Antigen/immunology ; Humans ; Immune Checkpoint Inhibitors ; Immune Evasion ; Immunity/immunology ; Immunity/physiology ; Immunotherapy ; Neoplasms/immunology ; Neoplasms/therapy ; Organ Transplantation ; Programmed Cell Death 1 Receptor/chemistry ; Programmed Cell Death 1 Receptor/immunology
    Chemical Substances B7-1 Antigen ; B7-H1 Antigen ; Immune Checkpoint Inhibitors ; Programmed Cell Death 1 Receptor
    Language English
    Publishing date 2020-11-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
    ZDB-ID 2036490-8
    ISSN 1471-499X ; 1471-4914
    ISSN (online) 1471-499X
    ISSN 1471-4914
    DOI 10.1016/j.molmed.2020.10.004
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 4345: Show issues Location:
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  4. Article ; Online: A SOX9-B7x axis safeguards dedifferentiated tumor cells from immune surveillance to drive breast cancer progression.

    Liu, Yu / John, Peter / Nishitani, Kenta / Cui, Jihong / Nishimura, Christopher D / Christin, John R / Couturier, Nicole / Ren, Xiaoxin / Wei, Yao / Pulanco, Marc C / Galbo, Phillip M / Zhang, Xusheng / Fu, Wenyan / Cui, Wei / Bartholdy, Boris A / Zheng, Deyou / Lauvau, Gregoire / Fineberg, Susan A / Oktay, Maja H /
    Zang, Xingxing / Guo, Wenjun

    Developmental cell

    2023  Volume 58, Issue 23, Page(s) 2700–2717.e12

    Abstract: How dedifferentiated stem-like tumor cells evade immunosurveillance remains poorly understood. We show that the lineage-plasticity regulator SOX9, which is upregulated in dedifferentiated tumor cells, limits the number of infiltrating T lymphocytes in ... ...

    Abstract How dedifferentiated stem-like tumor cells evade immunosurveillance remains poorly understood. We show that the lineage-plasticity regulator SOX9, which is upregulated in dedifferentiated tumor cells, limits the number of infiltrating T lymphocytes in premalignant lesions of mouse basal-like breast cancer. SOX9-mediated immunosuppression is required for the progression of in situ tumors to invasive carcinoma. SOX9 induces the expression of immune checkpoint B7x/B7-H4 through STAT3 activation and direct transcriptional regulation. B7x is upregulated in dedifferentiated tumor cells and protects them from immunosurveillance. B7x also protects mammary gland regeneration in immunocompetent mice. In advanced tumors, B7x targeting inhibits tumor growth and overcomes resistance to anti-PD-L1 immunotherapy. In human breast cancer, SOX9 and B7x expression are correlated and associated with reduced CD8
    MeSH term(s) Animals ; Female ; Humans ; Mice ; Breast Neoplasms ; CD8-Positive T-Lymphocytes ; Immunosuppression Therapy ; SOX9 Transcription Factor ; V-Set Domain-Containing T-Cell Activation Inhibitor 1/metabolism
    Chemical Substances SOX9 protein, human ; SOX9 Transcription Factor ; V-Set Domain-Containing T-Cell Activation Inhibitor 1 ; Vtcn1 protein, mouse
    Language English
    Publishing date 2023-11-13
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2054967-2
    ISSN 1878-1551 ; 1534-5807
    ISSN (online) 1878-1551
    ISSN 1534-5807
    DOI 10.1016/j.devcel.2023.10.010
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    Zs.A 5742: Show issues Location:
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    Zs.MG 76: Show issues

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  5. Article ; Online: A Virion-Based Assay for Glycoprotein Thermostability Reveals Key Determinants of Filovirus Entry and Its Inhibition.

    Bortz, Robert H / Wong, Anthony C / Grodus, Michael G / Recht, Hannah S / Pulanco, Marc C / Lasso, Gorka / Anthony, Simon J / Mittler, Eva / Jangra, Rohit K / Chandran, Kartik

    Journal of virology

    2020  Volume 94, Issue 18

    Abstract: Ebola virus (EBOV) entry into cells is mediated by its spike glycoprotein (GP). Following attachment and internalization, virions traffic to late endosomes where GP is cleaved by host cysteine proteases. Cleaved GP then binds its cellular receptor, ... ...

    Abstract Ebola virus (EBOV) entry into cells is mediated by its spike glycoprotein (GP). Following attachment and internalization, virions traffic to late endosomes where GP is cleaved by host cysteine proteases. Cleaved GP then binds its cellular receptor, Niemann-Pick C1. In response to an unknown cellular trigger, GP undergoes conformational rearrangements that drive fusion of viral and endosomal membranes. The temperature-dependent stability (thermostability) of the prefusion conformers of class I viral fusion glycoproteins, including those of filovirus GPs, has provided insights into their propensity to undergo fusion-related rearrangements. However, previously described assays have relied on soluble glycoprotein ectodomains. Here, we developed a simple enzyme-linked immunosorbent assay (ELISA)-based assay that uses the temperature-dependent loss of conformational epitopes to measure thermostability of GP embedded in viral membranes. The base and glycan cap subdomains of all filovirus GPs tested suffered a concerted loss of prefusion conformation at elevated temperatures but did so at different temperature ranges, indicating virus-specific differences in thermostability. Despite these differences, all of these GPs displayed reduced thermostability upon cleavage to GP conformers (GP
    MeSH term(s) Animals ; Binding Sites ; Biological Assay ; Chlorocebus aethiops ; Clomiphene/chemistry ; Clomiphene/pharmacology ; Ebolavirus/chemistry ; Ebolavirus/drug effects ; Ebolavirus/genetics ; Ebolavirus/metabolism ; Epitopes/chemistry ; Epitopes/genetics ; Epitopes/metabolism ; Hot Temperature ; Hydrogen-Ion Concentration ; Molecular Docking Simulation ; Niemann-Pick C1 Protein/antagonists & inhibitors ; Niemann-Pick C1 Protein/chemistry ; Niemann-Pick C1 Protein/genetics ; Niemann-Pick C1 Protein/metabolism ; Protein Binding/drug effects ; Protein Interaction Domains and Motifs ; Protein Stability ; Protein Structure, Tertiary ; Receptors, Virus/antagonists & inhibitors ; Receptors, Virus/chemistry ; Receptors, Virus/genetics ; Receptors, Virus/metabolism ; Tamoxifen/analogs & derivatives ; Tamoxifen/chemistry ; Tamoxifen/pharmacology ; Toremifene/chemistry ; Toremifene/pharmacology ; Vero Cells ; Viral Envelope Proteins/antagonists & inhibitors ; Viral Envelope Proteins/chemistry ; Viral Envelope Proteins/genetics ; Viral Envelope Proteins/metabolism ; Viral Fusion Proteins/antagonists & inhibitors ; Viral Fusion Proteins/chemistry ; Viral Fusion Proteins/genetics ; Viral Fusion Proteins/metabolism ; Virion/chemistry ; Virion/drug effects ; Virion/genetics ; Virion/metabolism
    Chemical Substances Epitopes ; Niemann-Pick C1 Protein ; Receptors, Virus ; Viral Envelope Proteins ; Viral Fusion Proteins ; envelope glycoprotein, Ebola virus ; Tamoxifen (094ZI81Y45) ; Clomiphene (1HRS458QU2) ; Toremifene (7NFE54O27T) ; Ospemifene (B0P231ILBK)
    Language English
    Publishing date 2020-08-31
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.00336-20
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 609: Show issues Location:
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  6. Article ; Online: Complement Protein C1q Enhances Macrophage Foam Cell Survival and Efferocytosis.

    Pulanco, Marc C / Cosman, Jason / Ho, Minh-Minh / Huynh, Jessica / Fing, Karina / Turcu, Jacqueline / Fraser, Deborah A

    Journal of immunology (Baltimore, Md. : 1950)

    2017  Volume 198, Issue 1, Page(s) 472–480

    Abstract: In the atherosclerotic lesion, macrophages ingest high levels of damaged modified low-density lipoproteins (LDLs), generating macrophage foam cells. Foam cells undergo apoptosis and, if not efficiently cleared by efferocytosis, can undergo secondary ... ...

    Abstract In the atherosclerotic lesion, macrophages ingest high levels of damaged modified low-density lipoproteins (LDLs), generating macrophage foam cells. Foam cells undergo apoptosis and, if not efficiently cleared by efferocytosis, can undergo secondary necrosis, leading to plaque instability and rupture. As a component of the innate immune complement cascade, C1q recognizes and opsonizes modified forms of LDL, such as oxidized or acetylated LDL, and promotes ingestion by macrophages in vitro. C1q was shown to be protective in an atherosclerosis model in vivo. Therefore, this study aimed to investigate whether ingestion of modified LDL in the presence of C1q alters macrophage foam cell survival or function. In an unbiased transcriptome analysis, C1q was shown to modulate expression of clusters of genes involved in cell death and apoptosis pathways in human monocyte-derived macrophages ingesting modified LDL; this was validated by quantitative PCR in human and murine macrophages. C1q downregulated levels and activity of active caspase-3 and PARP-1 in human and mouse macrophages during ingestion of modified LDL. This led to a measurable increase in survival and decrease in cell death, as measured by alamarBlue and propidium iodide assays, respectively. C1q opsonization also increased phagocytosis and efferocytosis in macrophage foam cells. These data suggest that C1q promotes macrophage survival during ingestion of excess cholesterol, as well as improves foam cell efferocytic function. This may be important in slowing disease progression and provides insight into the protective role of C1q in early atherosclerosis.
    MeSH term(s) Animals ; Apoptosis/immunology ; Atherosclerosis/immunology ; Atherosclerosis/pathology ; Cell Survival/immunology ; Complement C1q/immunology ; Foam Cells/immunology ; Humans ; Mice ; Polymerase Chain Reaction
    Chemical Substances Complement C1q (80295-33-6)
    Language English
    Publishing date 2017-01-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3056-9
    ISSN 1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
    ISSN (online) 1550-6606
    ISSN 0022-1767 ; 1048-3233 ; 1047-7381
    DOI 10.4049/jimmunol.1601445
    Database MEDical Literature Analysis and Retrieval System OnLINE

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