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KSHV infection of B cells primes protective T cell responses in humanized mice

Nature communications, 2024-06, Vol.15 (1), p.4841, Article 4841

2024

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Altered EBV specific immune control in multiple sclerosis

Journal of neuroimmunology, 2024-05, Vol.390, p.578343-578343, Article 578343

Münz, Christian

2024

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Modulation of Epstein-Barr-Virus (EBV)-Associated Cancers by Co-Infections

Cancers, 2023-12, Vol.15 (24), p.5739

Münz, Christian

2023

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The autophagy machinery interacts with EBV capsids during viral envelope release

Proceedings of the National Academy of Sciences - PNAS, 2023-08, Vol.120 (34), p.e2211281120-e2211281120

2023

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MHC class II‐deficient mice allow functional human CD4+ T‐cell development

European journal of immunology, 2023-07, Vol.53 (7), p.e2250313-n/a

2023

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Distinctive Kaposi Sarcoma-Associated Herpesvirus Serological Profile during Acute Plasmodium falciparum Malaria Episodes

International journal of molecular sciences, 2023-04, Vol.24 (7), p.6711

2023

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Epstein-Barr virus as a leading cause of multiple sclerosis: mechanisms and implications

Nature reviews. Neurology, 2023-03, Vol.19 (3), p.160-171

2023

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Immune checkpoints in T cells during oncogenic γ‐herpesvirus infections

Journal of medical virology, 2023-01, Vol.95 (1), p.e27840-n/a

Münz, Christian

2023

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Co-Infection of the Epstein-Barr Virus and the Kaposi Sarcoma-Associated Herpesvirus

Viruses, 2022-12, Vol.14 (12), p.2709

2022

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Epstein Barr virus-mediated transformation of B cells from XIAP-deficient patients leads to increased expression of the tumor suppressor CADM1

Cell death & disease, 2022-10, Vol.13 (10), p.892-892, Article 892

2022

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Altered Immune Response to the Epstein–Barr Virus as a Prerequisite for Multiple Sclerosis

Cells (Basel, Switzerland), 2022-09, Vol.11 (17), p.2757

2022

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Evolution of functional antibodies following acute Epstein-Barr virus infection

PLoS pathogens, 2022-09, Vol.18 (9), p.e1010738-e1010738

2022

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Reduced IRF4 expression promotes lytic phenotype in Type 2 EBV-infected B cells

PLoS pathogens, 2022-04, Vol.18 (4), p.e1010453-e1010453

2022

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EBV+ tumors exploit tumor cell-intrinsic and -extrinsic mechanisms to produce regulatory T cell-recruiting chemokines CCL17 and CCL22

PLoS pathogens, 2022-01, Vol.18 (1), p.e1010200-e1010200

2022

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Reduced frequency of cytotoxic CD56dim CD16+ NK cells leads to impaired antibody-dependent degranulation in EBV-positive classical Hodgkin lymphoma

Cancer Immunology, Immunotherapy, 2022, Vol.71 (1), p.13-24

2022

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Co-Stimulatory Molecules during Immune Control of Epstein Barr Virus Infection

Biomolecules (Basel, Switzerland), 2021-12, Vol.12 (1), p.38

Münz, Christian

2021

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PLK1‐dependent phosphorylation restrains EBNA2 activity and lymphomagenesis in EBV‐infected mice

EMBO reports, 2021-12, Vol.22 (12), p.e53007-n/a

2021

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Cytotoxic CD4+ T-cells specific for EBV capsid antigen BORF1 are maintained in long-term latently infected healthy donors

PLoS pathogens, 2021-12, Vol.17 (12), p.e1010137-e1010137

2021

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Interplay between IL-10, IFN-γ, IL-17A and PD-1 Expressing EBNA1-Specific CD4+ and CD8+ T Cell Responses in the Etiologic Pathway to Endemic Burkitt Lymphoma

Cancers, 2021-10, Vol.13 (21), p.5375

2021

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Epstein Barr Virus Exploits Genetic Susceptibility to Increase Multiple Sclerosis Risk

Microorganisms (Basel), 2021-10, Vol.9 (11), p.2191

2021

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Natural Killer Cell Responses during Human γ-Herpesvirus Infections

Vaccines (Basel), 2021-06, Vol.9 (6), p.655

Münz, Christian

2021

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CD27 is required for protective lytic EBV antigen–specific CD8+ T-cell expansion

Blood, 2021-06, Vol.137 (23), p.3225-3236

2021

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Roles of Lytic Viral Replication and Co-Infections in the Oncogenesis and Immune Control of the Epstein–Barr Virus

Cancers, 2021-05, Vol.13 (9), p.2275

2021

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Regulation of the Macroautophagic Machinery, Cellular Differentiation, and Immune Responses by Human Oncogenic γ-Herpesviruses

Viruses, 2021-05, Vol.13 (5), p.859

Münz, Christian

2021

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KSHV infection drives poorly cytotoxic CD56-negative natural killer cell differentiation in vivo upon KSHV/EBV dual infection

Cell reports (Cambridge), 2021-05, Vol.35 (5), p.109056-109056, Article 109056

2021

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KSHV infection of B cells primes protective T cell responses in humanized mice

Altered EBV specific immune control in multiple sclerosis

Modulation of Epstein-Barr-Virus (EBV)-Associated Cancers by Co-Infections

The autophagy machinery interacts with EBV capsids during viral envelope release

MHC class II‐deficient mice allow functional human CD4+ T‐cell development

Distinctive Kaposi Sarcoma-Associated Herpesvirus Serological Profile during Acute Plasmodium falciparum Malaria Episodes

Epstein-Barr virus as a leading cause of multiple sclerosis: mechanisms and implications

Immune checkpoints in T cells during oncogenic γ‐herpesvirus infections

Co-Infection of the Epstein-Barr Virus and the Kaposi Sarcoma-Associated Herpesvirus

Epstein Barr virus-mediated transformation of B cells from XIAP-deficient patients leads to increased expression of the tumor suppressor CADM1

Altered Immune Response to the Epstein–Barr Virus as a Prerequisite for Multiple Sclerosis

Evolution of functional antibodies following acute Epstein-Barr virus infection

Reduced IRF4 expression promotes lytic phenotype in Type 2 EBV-infected B cells

EBV+ tumors exploit tumor cell-intrinsic and -extrinsic mechanisms to produce regulatory T cell-recruiting chemokines CCL17 and CCL22

Reduced frequency of cytotoxic CD56dim CD16+ NK cells leads to impaired antibody-dependent degranulation in EBV-positive classical Hodgkin lymphoma

Co-Stimulatory Molecules during Immune Control of Epstein Barr Virus Infection

PLK1‐dependent phosphorylation restrains EBNA2 activity and lymphomagenesis in EBV‐infected mice

Cytotoxic CD4+ T-cells specific for EBV capsid antigen BORF1 are maintained in long-term latently infected healthy donors

Interplay between IL-10, IFN-γ, IL-17A and PD-1 Expressing EBNA1-Specific CD4+ and CD8+ T Cell Responses in the Etiologic Pathway to Endemic Burkitt Lymphoma

Epstein Barr Virus Exploits Genetic Susceptibility to Increase Multiple Sclerosis Risk

Natural Killer Cell Responses during Human γ-Herpesvirus Infections

CD27 is required for protective lytic EBV antigen–specific CD8+ T-cell expansion

Roles of Lytic Viral Replication and Co-Infections in the Oncogenesis and Immune Control of the Epstein–Barr Virus

Regulation of the Macroautophagic Machinery, Cellular Differentiation, and Immune Responses by Human Oncogenic γ-Herpesviruses

KSHV infection drives poorly cytotoxic CD56-negative natural killer cell differentiation in vivo upon KSHV/EBV dual infection

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