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3. Replication of Influenza A Virus in Secondary Lymphatic Tissue Contributes to Innate Immune Activation

Author

Friedrich, Sarah-Kim, Schmitz, Rosa, Bergerhausen, Michael, Lang, Judith, Duhan, Vikas, Hardt, Cornelia, Tenbusch, Matthias, Prinz, Marco, Asano, Kenichi, Bhat, Hilal, Hamdan, Thamer A., Lang, Philipp Alexander, and Lang, Karl Sebastian

Subjects
enforced viral replication, Medizinische Fakultät » Universitätsklinikum Essen » Institut für Immunologie, innate immune activation, viruses, Medizin, Medicine, ddc:610, Influenza virus, Article
Abstract

The replication of viruses in secondary lymphoid organs guarantees sufficient amounts of pattern-recognition receptor ligands and antigens to activate the innate and adaptive immune system. Viruses with broad cell tropism usually replicate in lymphoid organs, however, whether a virus with a narrow tropism relies on replication in the secondary lymphoid organs to activate the immune system remains not well studied. In this study, we used the artificial intravenous route of infection to determine whether Influenza A virus (IAV) replication can occur in secondary lymphatic organs (SLO) and whether such replication correlates with innate immune activation. Indeed, we found that IAV replicates in secondary lymphatic tissue. IAV replication was dependent on the expression of Sialic acid residues in antigen-presenting cells and on the expression of the interferon-inhibitor UBP43 (Usp18). The replication of IAV correlated with innate immune activation, resulting in IAV eradication. The genetic deletion of Usp18 curbed IAV replication and limited innate immune activation. In conclusion, we found that IAV replicates in SLO, a mechanism which allows innate immune activation.

Published
2021

5. Targeting HDACs in Pancreatic Neuroendocrine Tumor Models

Author

Schmitz, Rosa Lynn, primary, Weissbach, Julia, additional, Kleilein, Jan, additional, Bell, Jessica, additional, Hüttelmaier, Stefan, additional, Viol, Fabrice, additional, Clauditz, Till, additional, Grabowski, Patricia, additional, Laumen, Helmut, additional, Rosendahl, Jonas, additional, Michl, Patrick, additional, Schrader, Jörg, additional, and Krug, Sebastian, additional

Published
2021
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6. Arenavirus Induced CCL5 Expression Causes NK Cell-Mediated Melanoma Regression

Author

Bhat, Hilal, primary, Zaun, Gregor, additional, Hamdan, Thamer A., additional, Lang, Judith, additional, Adomati, Tom, additional, Schmitz, Rosa, additional, Friedrich, Sarah-Kim, additional, Bergerhausen, Michael, additional, Cham, Lamin B., additional, Li, Fanghui, additional, Ali, Murtaza, additional, Zhou, Fan, additional, Khairnar, Vishal, additional, Duhan, Vikas, additional, Brandenburg, Tim, additional, Machlah, Yara Maria, additional, Schiller, Maximilian, additional, Berry, Arshia, additional, Xu, Haifeng, additional, Vollmer, Jörg, additional, Häussinger, Dieter, additional, Thier, Beatrice, additional, Pandyra, Aleksandra A., additional, Schadendorf, Dirk, additional, Paschen, Annette, additional, Schuler, Martin, additional, Lang, Philipp A., additional, and Lang, Karl S., additional

Published
2020
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7. Usp18 Expression in CD169+ Macrophages is Important for Strong Immune Response after Vaccination with VSV-EBOV

Author

Friedrich, Sarah-Kim, primary, Schmitz, Rosa, additional, Bergerhausen, Michael, additional, Lang, Judith, additional, Cham, Lamin B., additional, Duhan, Vikas, additional, Häussinger, Dieter, additional, Hardt, Cornelia, additional, Addo, Marylyn, additional, Prinz, Marco, additional, Asano, Kenichi, additional, Lang, Philipp Alexander, additional, and Lang, Karl Sebastian, additional

Published
2020
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8. Usp18 Expression in CD169 + Macrophages is Important for Strong Immune Response after Vaccination with VSV-EBOV.

Author

Friedrich SK, Schmitz R, Bergerhausen M, Lang J, Cham LB, Duhan V, Häussinger D, Hardt C, Addo M, Prinz M, Asano K, Lang PA, and Lang KS

Abstract

Ebola virus epidemics can be effectively limited by the VSV-EBOV vaccine (Ervebo) due to its rapid protection abilities; however, side effects prevent the broad use of VSV-EBOV as vaccine. Mechanisms explaining the efficient immune activation after single injection with the VSV-EBOV vaccine remain mainly unknown. Here, using the clinically available VSV-EBOV vaccine (Ervebo), we show that the cell-intrinsic expression of the interferon-inhibitor Usp18 in CD169 + macrophages is one important factor modulating the anti-Ebola virus immune response. The absence of Usp18 in CD169 + macrophages led to the reduced local replication of VSV-EBOV followed by a diminished innate as well as adaptive immune response. In line, CD169 -Cre +/ki x Usp18 fl/fl mice showed reduced innate and adaptive immune responses against the VSV wildtype strain and died quickly after infection, suggesting that a lack of Usp18 makes mice more susceptible to the side effects of the VSV vector. In conclusion, our study shows that Usp18 expression in CD169 + macrophages is one important surrogate marker for effective vaccination against VSV-EBOV, and probably other VSV-based vaccines also.

Published
2020
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