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Article ; Online: PD-1 Immune Checkpoint Blockade and PSGL-1 Inhibition Synergize to Reinvigorate Exhausted T Cells.

Viramontes, Karla M / Neubert, Emily N / DeRogatis, Julia M / Tinoco, Roberto

2022 Volume 13, Page(s) 869768

Abstract: Chronic viral infections where the antigen persists long-term, induces an exhaustion phenotype in responding T cells. It is now evident that immune checkpoints on T cells including PD-1, CTLA-4, and PSGL-1 ( ...

Abstract	Chronic viral infections where the antigen persists long-term, induces an exhaustion phenotype in responding T cells. It is now evident that immune checkpoints on T cells including PD-1, CTLA-4, and PSGL-1 (
MeSH term(s)	CD8-Positive T-Lymphocytes/immunology ; Hepatitis A Virus Cellular Receptor 2/immunology ; Humans ; Immune Checkpoint Inhibitors/pharmacology ; Lymphocytic Choriomeningitis/drug therapy ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus/immunology ; Membrane Glycoproteins/antagonists & inhibitors ; Membrane Glycoproteins/immunology ; Programmed Cell Death 1 Receptor/antagonists & inhibitors ; Programmed Cell Death 1 Receptor/immunology
Chemical Substances	Hepatitis A Virus Cellular Receptor 2 ; Immune Checkpoint Inhibitors ; Membrane Glycoproteins ; P-selectin ligand protein ; PDCD1 protein, human ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2022-06-14
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.869768
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Cell-Intrinsic CD38 Expression Sustains Exhausted CD8

DeRogatis, Julia M / Neubert, Emily N / Viramontes, Karla M / Henriquez, Monique L / Nicholas, Dequina A / Tinoco, Roberto

Journal of virology

2023 Volume 97, Issue 4, Page(s) e0022523

Abstract: Acute and chronic viral infections result in the differentiation of effector and exhausted T cells with functional and phenotypic differences that dictate whether the infection is cleared or progresses to chronicity. High CD38 expression has been ... ...

Abstract	Acute and chronic viral infections result in the differentiation of effector and exhausted T cells with functional and phenotypic differences that dictate whether the infection is cleared or progresses to chronicity. High CD38 expression has been observed on CD8
MeSH term(s)	CD8-Positive T-Lymphocytes/metabolism ; CD8-Positive T-Lymphocytes/virology ; Cell Differentiation/genetics ; Lymphocytic Choriomeningitis/metabolism ; Lymphocytic choriomeningitis virus/genetics ; Persistent Infection ; Animals ; Mice ; Cell Survival/genetics ; Up-Regulation ; Cell Proliferation/genetics
Chemical Substances	Cd38 protein, mouse (EC 3.2.2.5)
Language	English
Publishing date	2023-04-11
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural
ZDB-ID	80174-4
ISSN	1098-5514 ; 0022-538X
ISSN (online)	1098-5514
ISSN	0022-538X
DOI	10.1128/jvi.00225-23
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Article ; Online: PSGL-1 Immune Checkpoint Inhibition for CD4

DeRogatis, Julia M / Viramontes, Karla M / Neubert, Emily N / Tinoco, Roberto

Frontiers in immunology

2021 Volume 12, Page(s) 636238

Abstract: Immune checkpoint inhibition targeting T cells has shown tremendous promise in the treatment of many cancer types and are now standard therapies for patients. While standard therapies have focused on PD-1 and CTLA-4 blockade, additional immune ... ...

Abstract	Immune checkpoint inhibition targeting T cells has shown tremendous promise in the treatment of many cancer types and are now standard therapies for patients. While standard therapies have focused on PD-1 and CTLA-4 blockade, additional immune checkpoints have shown promise in promoting anti-tumor immunity. PSGL-1, primarily known for its role in cellular migration, has also been shown to function as a negative regulator of CD4
MeSH term(s)	Animals ; CD4-Positive T-Lymphocytes/drug effects ; CD4-Positive T-Lymphocytes/immunology ; CD4-Positive T-Lymphocytes/metabolism ; Humans ; Immune Checkpoint Inhibitors/adverse effects ; Immune Checkpoint Inhibitors/therapeutic use ; Lymphocytes, Tumor-Infiltrating/drug effects ; Lymphocytes, Tumor-Infiltrating/immunology ; Lymphocytes, Tumor-Infiltrating/metabolism ; Membrane Glycoproteins/antagonists & inhibitors ; Membrane Glycoproteins/genetics ; Membrane Glycoproteins/immunology ; Membrane Glycoproteins/metabolism ; Mice, Knockout ; Molecular Targeted Therapy ; Neoplasms/drug therapy ; Neoplasms/genetics ; Neoplasms/immunology ; Neoplasms/metabolism ; Phenotype ; Signal Transduction ; Tumor Microenvironment ; Mice
Chemical Substances	Immune Checkpoint Inhibitors ; Membrane Glycoproteins ; P-selectin ligand protein
Language	English
Publishing date	2021-02-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.636238
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Article ; Online: Targeting the PSGL-1 Immune Checkpoint Promotes Immunity to PD-1-Resistant Melanoma.

DeRogatis, Julia M / Viramontes, Karla M / Neubert, Emily N / Henriquez, Monique L / Guerrero-Juarez, Christian F / Tinoco, Roberto

Cancer immunology research

2022 Volume 10, Issue 5, Page(s) 612–625

Abstract: Immune-checkpoint inhibitors have had impressive efficacy in some patients with cancer, reinvigorating long-term durable immune responses against tumors. Despite the clinical success of these therapies, most patients with cancer continue to be ... ...

Abstract	Immune-checkpoint inhibitors have had impressive efficacy in some patients with cancer, reinvigorating long-term durable immune responses against tumors. Despite the clinical success of these therapies, most patients with cancer continue to be unresponsive to these treatments, highlighting the need for novel therapeutic options. Although P-selectin glycoprotein ligand-1 (PSGL-1) has been shown to inhibit immune responses in a variety of disease models, previous work has yet to address whether PSGL-1 can be targeted therapeutically to promote antitumor immunity. Using an aggressive melanoma tumor model, we targeted PSGL-1 in tumor-bearing mice and found increased effector CD4+ and CD8+ T-cell responses and decreased regulatory T cells (Treg) in tumors. T cells exhibited increased effector function, activation, and proliferation, which delayed tumor growth in mice after anti-PSGL-1 treatment. Targeting PD-1 in PSGL-1-deficient, tumor-bearing mice led to an increased frequency of mice with complete tumor eradication. Targeting both PSGL-1 and PD-1 in wild-type tumor-bearing mice also showed enhanced antitumor immunity and slowed melanoma tumor growth. Our findings showed that therapeutically targeting the PSGL-1 immune checkpoint can reinvigorate antitumor immunity and suggest that targeting PSGL-1 may represent a new therapeutic strategy for cancer treatment.
MeSH term(s)	Animals ; Cell Line, Tumor ; Humans ; Immune Checkpoint Inhibitors ; Melanoma/drug therapy ; Membrane Glycoproteins ; Mice ; Mice, Inbred C57BL ; Programmed Cell Death 1 Receptor
Chemical Substances	Immune Checkpoint Inhibitors ; Membrane Glycoproteins ; P-selectin ligand protein ; Programmed Cell Death 1 Receptor
Language	English
Publishing date	2022-03-18
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2732489-8
ISSN	2326-6074 ; 2326-6066
ISSN (online)	2326-6074
ISSN	2326-6066
DOI	10.1158/2326-6066.CIR-21-0690
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Article ; Online: HMGB2 regulates the differentiation and stemness of exhausted CD8

Neubert, Emily N / DeRogatis, Julia M / Lewis, Sloan A / Viramontes, Karla M / Ortega, Pedro / Henriquez, Monique L / Buisson, Rémi / Messaoudi, Ilhem / Tinoco, Roberto

Nature communications

2023 Volume 14, Issue 1, Page(s) 5631

Abstract: Chronic infections and cancers evade the host immune system through mechanisms that induce T cell exhaustion. The heterogeneity within the exhausted ... ...

Abstract	Chronic infections and cancers evade the host immune system through mechanisms that induce T cell exhaustion. The heterogeneity within the exhausted CD8
MeSH term(s)	Humans ; CD8-Positive T-Lymphocytes ; HMGB2 Protein/genetics ; Persistent Infection ; Cell Differentiation ; Virus Diseases ; Neoplasms
Chemical Substances	HMGB2 Protein
Language	English
Publishing date	2023-09-13
Publishing country	England
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-41352-0
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Article ; Online: Synergism between the tyrosine kinase inhibitor sunitinib and Anti-TNF antibody protects against lethal dengue infection.

Branche, Emilie / Tang, William Weihao / Viramontes, Karla M / Young, Matthew Perry / Sheets, Nicholas / Joo, Yunichel / Nguyen, Anh-Viet T / Shresta, Sujan

Antiviral research

2018 Volume 158, Page(s) 1–7

Abstract: Dengue virus (DENV) currently circulates in more than 100 countries and causes an estimated 390 million infections per year. While most cases manifest as a self-resolving fever, ∼1.5% of infections develop into a more severe dengue hemorrhagic fever/ ... ...

Abstract	Dengue virus (DENV) currently circulates in more than 100 countries and causes an estimated 390 million infections per year. While most cases manifest as a self-resolving fever, ∼1.5% of infections develop into a more severe dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS), which causes ∼20,000 deaths annually. The underlying pathological feature of DHF/DSS, also known as Severe Dengue, is an acute increase in vascular permeability leading to hypovolemia and shock. Angiogenic factors and cytokines, such as vascular endothelial growth factor (VEGF) and tumor necrosis factor (TNF), have been implicated in the increased vascular permeability, suggesting a potential therapeutic strategy for Severe Dengue. Here, we employed a mouse model of antibody-dependent enhancement of DENV infection, which recapitulates the fatal capillary leakage and shock of human Severe Dengue, to investigate the effects of approved VEGF- and TNF-targeting drugs. DENV infection caused a significant increase in serum VEGF levels within 2 days and resulted in ∼80% mortality within 8 days of infection. Treatment of mice with sunitinib, a VEGF receptor tyrosine kinase inhibitor, once (day 2) or twice (days 1 and 2) post-infection reduced mortality by 50-80% compared with untreated mice. Notably, sunitinib treatment decreased serum TNF levels, white blood cell counts, and hematocrit levels relative to untreated mice, but had only marginal effects on tissue viral burden. Combination therapy with anti-TNF antibody and sunitinib significantly reduced vascular leakage and synergized to provide superior protection from lethal DENV infection compared with either agent alone. These data suggest that a two-pronged anti-angiogenic and anti-inflammatory approach may be useful for the rapid treatment of DHF/DSS.
MeSH term(s)	Angiogenesis Inducing Agents ; Animals ; Antibodies, Viral/pharmacology ; Antibody-Dependent Enhancement ; Capillary Permeability/drug effects ; Cell Line ; Culicidae ; Dengue/drug therapy ; Dengue/virology ; Dengue Virus/pathogenicity ; Disease Models, Animal ; Drug Combinations ; Enzyme Inhibitors/pharmacology ; Female ; Male ; Mice ; Protein-Tyrosine Kinases/antagonists & inhibitors ; RNA, Viral/isolation & purification ; Severe Dengue/prevention & control ; Sunitinib/pharmacology ; Survival Rate ; Tumor Necrosis Factor-alpha/drug effects ; Vascular Endothelial Growth Factor A/blood ; Viral Load
Chemical Substances	Angiogenesis Inducing Agents ; Antibodies, Viral ; Drug Combinations ; Enzyme Inhibitors ; RNA, Viral ; Tumor Necrosis Factor-alpha ; Vascular Endothelial Growth Factor A ; Protein-Tyrosine Kinases (EC 2.7.10.1) ; Sunitinib (V99T50803M)
Language	English
Publishing date	2018-07-30
Publishing country	Netherlands
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	306628-9
ISSN	1872-9096 ; 0166-3542
ISSN (online)	1872-9096
ISSN	0166-3542
DOI	10.1016/j.antiviral.2018.07.022
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Zs.A 1627: Show issues

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Article ; Online: The Ability of Zika virus Intravenous Immunoglobulin to Protect From or Enhance Zika Virus Disease.

Pinto, Amelia K / Hassert, Mariah / Han, Xiaobing / Barker, Douglas / Carnelley, Trevor / Branche, Emilie / Steffen, Tara L / Stone, E Taylor / Geerling, Elizabeth / Viramontes, Karla M / Nykiforuk, Cory / Toth, Derek / Shresta, Sujan / Kodihalli, Shantha / Brien, James D

Frontiers in immunology

2021 Volume 12, Page(s) 717425

Abstract: The closely related flaviviruses, dengue and Zika, cause significant human disease throughout the world. While cross-reactive antibodies have been demonstrated to have the capacity to potentiate disease or mediate protection during flavivirus infection, ... ...

Abstract	The closely related flaviviruses, dengue and Zika, cause significant human disease throughout the world. While cross-reactive antibodies have been demonstrated to have the capacity to potentiate disease or mediate protection during flavivirus infection, the mechanisms responsible for this dichotomy are still poorly understood. To understand how the human polyclonal antibody response can protect against, and potentiate the disease in the context of dengue and Zika virus infection we used intravenous hyperimmunoglobulin (IVIG) preparations in a mouse model of the disease. Three IVIGs (ZIKV-IG, Control-Ig and Gamunex
MeSH term(s)	Animals ; Antibodies, Neutralizing/immunology ; Antibodies, Viral/immunology ; Cell Line ; Cross Reactions/immunology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Host-Pathogen Interactions/immunology ; Humans ; Immunoglobulins, Intravenous/therapeutic use ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Mice, Knockout ; Neutralization Tests ; Zika Virus/immunology ; Zika Virus Infection/blood ; Zika Virus Infection/drug therapy ; Zika Virus Infection/immunology ; Zika Virus Infection/virology
Chemical Substances	Antibodies, Neutralizing ; Antibodies, Viral ; Immunoglobulins, Intravenous
Language	English
Publishing date	2021-09-06
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2021.717425
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Article ; Online: SREBP2-dependent lipid gene transcription enhances the infection of human dendritic cells by Zika virus.

Nature communications

2022 Volume 13, Issue 1, Page(s) 5341

Abstract: The emergence of Zika virus (ZIKV) as a global health threat has highlighted the unmet need for ZIKV-specific vaccines and antiviral treatments. ZIKV infects dendritic cells (DC), which have pivotal functions in activating innate and adaptive antiviral ... ...

Abstract	The emergence of Zika virus (ZIKV) as a global health threat has highlighted the unmet need for ZIKV-specific vaccines and antiviral treatments. ZIKV infects dendritic cells (DC), which have pivotal functions in activating innate and adaptive antiviral responses; however, the mechanisms by which DC function is subverted to establish ZIKV infection are unclear. Here we develop a genomics profiling method that enables discrete analysis of ZIKV-infected versus neighboring, uninfected primary human DCs to increase the sensitivity and specificity with which ZIKV-modulated pathways can be identified. The results show that ZIKV infection specifically increases the expression of genes enriched for lipid metabolism-related functions. ZIKV infection also increases the recruitment of sterol regulatory element-binding protein (SREBP) transcription factors to lipid gene promoters, while pharmacologic inhibition or genetic silencing of SREBP2 suppresses ZIKV infection of DCs. Our data thus identify SREBP2-activated transcription as a mechanism for promoting ZIKV infection amenable to therapeutic targeting.
MeSH term(s)	Antiviral Agents/pharmacology ; Dendritic Cells ; Humans ; Lipids ; Transcription, Genetic ; Zika Virus ; Zika Virus Infection
Chemical Substances	Antiviral Agents ; Lipids
Language	English
Publishing date	2022-09-12
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; 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/s41467-022-33041-1
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Article ; Online: A Zika virus mutation enhances transmission potential and confers escape from protective dengue virus immunity.

Regla-Nava, Jose Angel / Wang, Ying-Ting / Fontes-Garfias, Camila R / Liu, Yang / Syed, Thasneem / Susantono, Mercylia / Gonzalez, Andrew / Viramontes, Karla M / Verma, Shailendra Kumar / Kim, Kenneth / Landeras-Bueno, Sara / Huang, Chun-Teng / Prigozhin, Daniil M / Gleeson, Joseph G / Terskikh, Alexey V / Shi, Pei-Yong / Shresta, Sujan

Cell reports

2022 Volume 39, Issue 2, Page(s) 110655

Abstract: Zika virus (ZIKV) and dengue virus (DENV) are arthropod-borne pathogenic flaviviruses that co-circulate in many countries. To understand some of the pressures that influence ZIKV evolution, we mimic the natural transmission cycle by repeating serial ... ...

Abstract	Zika virus (ZIKV) and dengue virus (DENV) are arthropod-borne pathogenic flaviviruses that co-circulate in many countries. To understand some of the pressures that influence ZIKV evolution, we mimic the natural transmission cycle by repeating serial passaging of ZIKV through cultured mosquito cells and either DENV-naive or DENV-immune mice. Compared with wild-type ZIKV, the strains passaged under both conditions exhibit increased pathogenesis in DENV-immune mice. Application of reverse genetics identifies an isoleucine-to-valine mutation (I39V) in the NS2B proteins of both passaged strains that confers enhanced fitness and escape from pre-existing DENV immunity. Introduction of I39V or I39T, a naturally occurring homologous mutation detected in recent ZIKV isolates, increases the replication of wild-type ZIKV in human neuronal precursor cells and laboratory-raised mosquitoes. Our data indicate that ZIKV strains with enhanced transmissibility and pathogenicity can emerge in DENV-naive or -immune settings, and that NS2B-I39 mutants may represent ZIKV variants of interest.
MeSH term(s)	Animals ; Antibodies, Viral ; Cross Reactions ; Dengue ; Dengue Virus/genetics ; Mice ; Mutation/genetics ; Zika Virus/genetics ; Zika Virus Infection
Chemical Substances	Antibodies, Viral
Language	English
Publishing date	2022-04-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2022.110655
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Article ; Online: Detection of Zika virus in mouse mammary gland and breast milk.

Regla-Nava, Jose Angel / Viramontes, Karla M / Vozdolska, Teodora / Huynh, Anh-Thy / Villani, Tom / Gardner, Graeme / Johnson, Michael / Ferro, Pamela J / Shresta, Sujan / Kim, Kenneth

PLoS neglected tropical diseases

2019 Volume 13, Issue 2, Page(s) e0007080

Abstract: Clinical reports of Zika Virus (ZIKV) RNA detection in breast milk have been described, but evidence conflicts as to whether this RNA represents infectious virus. We infected post-parturient AG129 murine dams deficient in type I and II interferon ... ...

Abstract	Clinical reports of Zika Virus (ZIKV) RNA detection in breast milk have been described, but evidence conflicts as to whether this RNA represents infectious virus. We infected post-parturient AG129 murine dams deficient in type I and II interferon receptors with ZIKV. ZIKV RNA was detected in pup stomach milk clots (SMC) as early as 1 day post maternal infection (dpi) and persisted as late as 7 dpi. In mammary tissues, ZIKV replication was demonstrated by immunohistochemistry in multiple cell types including cells morphologically consistent with myoepithelial cells. No mastitis was seen histopathologically. In the SMC and tissues of the nursing pups, no infectious virus was detected via focus forming assay. However, serial passages of fresh milk supernatant yielded infectious virus, and immunohistochemistry showed ZIKV replication protein associated with degraded cells in SMC. These results suggest that breast milk may contain infectious ZIKV. However, breast milk transmission (BMT) does not occur in this mouse strain that is highly sensitive to ZIKV infection. These results suggest a low risk for breast milk transmission of ZIKV, and provide a platform for investigating ZIKV entry into milk and mechanisms which may prevent or permit BMT.
MeSH term(s)	Animals ; Brain/virology ; Female ; Mammary Glands, Animal/virology ; Mice ; Milk/virology ; Spleen/virology ; Zika Virus/isolation & purification ; Zika Virus Infection/blood ; Zika Virus Infection/virology
Language	English
Publishing date	2019-02-11
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2429704-5
ISSN	1935-2735 ; 1935-2735
ISSN (online)	1935-2735
ISSN	1935-2735
DOI	10.1371/journal.pntd.0007080
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