Quantum Dots for Tracking Dendritic Cells and Priming an Immune Response In Vitro and In Vivo

Polystyrene nanoplastics are internalized in zebrafish liver cells, accumulating in lysosomes, and in zebrafish larvae but do not affect the larval suvival to a lethal infection.

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Parvovirus H-1-Induced Tumor Cell Death Enhances Human Immune Response In Vitro via Increased Phagocytosis, Maturation, and Cross-Presentation by Dendritic Cells

Human Gene Therapy ◽

10.1089/hum.2005.16.ft-92 ◽

2005 ◽

Vol 0 (0) ◽

pp. 050701034702004

Author(s):

Markus H. Moehler ◽

Maja Zeidler ◽

Vanessa Wilsberg ◽

Jan J. Cornelis ◽

Thomas Woelfel ◽

...

Keyword(s):

Immune Response ◽

Cell Death ◽

Dendritic Cells ◽

Tumor Cell ◽

Tumor Cell Death ◽

Cross Presentation ◽

Human Immune Response ◽

Human Immune ◽

Immune Response In Vitro

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Bridging channel dendritic cells induce immunity to transfused red blood cells

Journal of Experimental Medicine ◽

10.1084/jem.20151720 ◽

2016 ◽

Vol 213 (6) ◽

pp. 887-896 ◽

Cited By ~ 54

Author(s):

Samuele Calabro ◽

Antonia Gallman ◽

Uthaman Gowthaman ◽

Dong Liu ◽

Pei Chen ◽

...

Keyword(s):

Immune Response ◽

T Cells ◽

Dendritic Cells ◽

T Cell ◽

Major Complication ◽

Life Saving ◽

T Cell Help ◽

Rbc Transfusion

Red blood cell (RBC) transfusion is a life-saving therapeutic tool. However, a major complication in transfusion recipients is the generation of antibodies against non-ABO alloantigens on donor RBCs, potentially resulting in hemolysis and renal failure. Long-lived antibody responses typically require CD4+ T cell help and, in murine transfusion models, alloimmunization requires a spleen. Yet, it is not known how RBC-derived antigens are presented to naive T cells in the spleen. We sought to answer whether splenic dendritic cells (DCs) were essential for T cell priming to RBC alloantigens. Transient deletion of conventional DCs at the time of transfusion or splenic DC preactivation before RBC transfusion abrogated T and B cell responses to allogeneic RBCs, even though transfused RBCs persisted in the circulation for weeks. Although all splenic DCs phagocytosed RBCs and activated RBC-specific CD4+ T cells in vitro, only bridging channel 33D1+ DCs were required for alloimmunization in vivo. In contrast, deletion of XCR1+CD8+ DCs did not alter the immune response to RBCs. Our work suggests that blocking the function of one DC subset during a narrow window of time during RBC transfusion could potentially prevent the detrimental immune response that occurs in patients who require lifelong RBC transfusion support.

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Preferential Infection of Mature Dendritic Cells by Mouse Hepatitis Virus Strain JHM

Journal of Virology ◽

10.1128/jvi.80.5.2506-2514.2006 ◽

2006 ◽

Vol 80 (5) ◽

pp. 2506-2514 ◽

Cited By ~ 26

Author(s):

Haixia Zhou ◽

Stanley Perlman

Keyword(s):

Immune Response ◽

Dendritic Cells ◽

Virus Strain ◽

Hepatitis Virus ◽

Ex Vivo ◽

Mouse Hepatitis Virus ◽

Demyelinating Diseases ◽

Immature Cells

ABSTRACT Mouse hepatitis virus strain JHM (MHV-JHM) causes acute encephalitis and acute and chronic demyelinating diseases in mice. Dendritic cells (DCs) are key cells in the initiation of innate and adaptive immune responses, and infection of these cells could potentially contribute to a dysregulated immune response; consistent with this, recent results suggest that DCs are readily infected by another strain of mouse hepatitis virus, the A59 strain (MHV-A59). Herein, we show that the JHM strain also productively infected DCs. Moreover, mature DCs were at least 10 times more susceptible than immature DCs to infection with MHV-JHM. DC function was impaired after MHV-JHM infection, resulting in decreased stimulation of CD8 T cells in vitro. Preferential infection of mature DCs was not due to differential expression of the MHV-JHM receptor CEACAM-1a on mature or immature cells or to differences in apoptosis. Although we could not detect infected DCs in vivo, both CD8+ and CD11b+ splenic DCs were susceptible to infection with MHV-JHM directly ex vivo. This preferential infection of mature DCs may inhibit the development of an efficient immune response to the virus.

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Parvovirus H-1-Induced Tumor Cell Death Enhances Human Immune Response In Vitro via Increased Phagocytosis, Maturation, and Cross-Presentation by Dendritic Cells

Human Gene Therapy ◽

10.1089/hum.2005.16.ft-102 ◽

2005 ◽

Vol 0 (0) ◽

pp. 050719131035001

Author(s):

Markus H. Moehler ◽

Maja Zeidler ◽

Vanessa Wilsberg ◽

Jan J. Cornelis ◽

Thomas Woelfel ◽

...

Keyword(s):

Immune Response ◽

Cell Death ◽

Dendritic Cells ◽

Tumor Cell ◽

Tumor Cell Death ◽

Cross Presentation ◽

Human Immune Response ◽

Human Immune ◽

Immune Response In Vitro

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Programming the anti-tumor immune response in vitro and its application to stop the growth of tumor cells and prolonging the lifespan of mice with carcinoma in vivo

ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia» ◽

10.25557/igpp.2017.4.8525 ◽

2017 ◽

pp. 67-73

Author(s):

С.В. Калиш ◽

С.В. Лямина ◽

А.А. Раецкая ◽

О.П. Буданова ◽

И.Ю. Малышев

Keyword(s):

Immune Response ◽

Tumor Growth ◽

Tumor Cells ◽

The Body ◽

Ehrlich Carcinoma ◽

Ec Cells ◽

Growth Of Tumor ◽

Immune Response In Vitro

Цель - представить доказательства правомерности гипотезы, что комбинированный пул репрограммированных in vitro макрофагов и лимфоцитов будет эффективно ограничивать пролиферацию опухолевых клеток in vitro , а при введении в организм будет существенно ограничивать развитие опухоли in vivo . Методика. Размножение опухолевых клеток инициировали in vitro путем добавления клеток карциномы Эрлиха (КЭ) в среду культивирования RPMI-1640. Развитие асцитной опухоли in vivo воспроизводили путем внутрибрюшной инъекции клеток КЭ мышам. Результаты. Установлено, что M3 макрофаги вместе с антиген-репрограммированными лимфоцитами оказывают выраженный противоопухолевый эффект и in vitro, и in vivo , который был существеннее противоопухолевого эффекта цисплатина. Заключение. Факты, свидетельствующие, что М3 макрофаги в сочетании с in vitro антиген-репрограммированными лимфоцитами значительно подавляют рост опухоли in vivo , делают перспективным разработку клинической версии биотехнологии ограничения роста опухоли путем предварительного программирования противоопухолевого иммунного ответа «в пробирке». Aim. To test a hypothesis that a combined pool of in vitro reprogrammed macrophages and lymphocytes will effectively limit growth of tumor cells in vitro , and injections of these cells into the body will considerably limit development of a tumor in vivo . Methods. Tumor growth was initiated in vitro by addition of Ehrlich carcinoma (EC) cells to the RPMI-1640 cell culture medium and in vivo by intraperitoneal injection of EC cells into mice. Results. M3 macrophages in combination with antigen-reprogrammed lymphocytes exerted a pronounced antitumor effect both in vitro and in vivo, which was superior to the effect of cisplatin. Conclusion. M3 macrophages in combination with in vitro antigen-reprogrammed lymphocytes significantly inhibited the tumor growth in vivo . This fact justifies development of a clinical version of the tumor growth restricting biotechnology using pre-programming of the antitumor immune response in vitro .

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