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1. Report on the Third Workshop on Sustainable Software for Science: Practice and Experiences (WSSSPE3)

Author

Katz, Daniel S, Choi, Sou-Cheng T, Niemeyer, Kyle E, Hetherington, James, Löffler, Frank, Gunter, Dan, Idaszak, Ray, Brandt, Steven R, Miller, Mark A, Gesing, Sandra, Jones, Nick D, Weber, Nic, Marru, Suresh, Allen, Gabrielle, Penzenstadler, Birgit, Venters, Colin C, Davis, Ethan, Hwang, Lorraine, Todorov, Ilian, Patra, Abani, and de Val-Borro, Miguel

Subjects
Bioengineering, Sustainable Cities and Communities
Published
2023

2. Report on the Third Workshop on Sustainable Software for Science: Practice and Experiences (WSSSPE3)

Author

Katz, Daniel S., Choi, Sou-Cheng T., Niemeyer, Kyle E., Hetherington, James, Löffler, Frank, Gunter, Dan, Idaszak, Ray, Brandt, Steven R., Miller, Mark A., Gesing, Sandra, Jones, Nick D., Weber, Nic, Marru, Suresh, Allen, Gabrielle, Penzenstadler, Birgit, Venters, Colin C., Davis, Ethan, Hwang, Lorraine, Todorov, Ilian, Patra, Abani, and de Val-Borro, Miguel

Subjects
Computer Science - Software Engineering
Abstract

This report records and discusses the Third Workshop on Sustainable Software for Science: Practice and Experiences (WSSSPE3). The report includes a description of the keynote presentation of the workshop, which served as an overview of sustainable scientific software. It also summarizes a set of lightning talks in which speakers highlighted to-the-point lessons and challenges pertaining to sustaining scientific software. The final and main contribution of the report is a summary of the discussions, future steps, and future organization for a set of self-organized working groups on topics including developing pathways to funding scientific software; constructing useful common metrics for crediting software stakeholders; identifying principles for sustainable software engineering design; reaching out to research software organizations around the world; and building communities for software sustainability. For each group, we include a point of contact and a landing page that can be used by those who want to join that group's future activities. The main challenge left by the workshop is to see if the groups will execute these activities that they have scheduled, and how the WSSSPE community can encourage this to happen.

Published
2016
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7. Inflammation drives thrombosis after Salmonella infection via CLEC-2 on platelets

Author

Hitchcock, Jessica R., Cook, Charlotte N., Bobat, Saeeda, Ross, Ewan A., Flores-Langarica, Adriana, Lowe, Kate L., Khan, Mahmood, Dominguez-Medina, C. Coral, Lax, Sian, Carvalho-Gaspar, Manuela, Hubscher, Stefan, Rainger, G. Ed, Cobbold, Mark, Buckley, Christopher D., Mitchell, Tim J., Mitchell, Andrea, Jones, Nick D., Van Rooijen, N., Kirchhofer, Daniel, Henderson, Ian R., Adams, David H., Watson, Steve P., and Cunningham, Adam F.

Subjects
Blood clot -- Development and progression, Inflammation -- Complications and side effects, Thrombosis -- Development and progression, Blood platelets -- Properties, Cell receptors -- Properties, Salmonellosis -- Complications and side effects, Health care industry
Abstract

Thrombosis is a common, life-threatening consequence of systemic infection; however, the underlying mechanisms that drive the formation of infection-associated thrombi are poorly understood. Here, using a mouse model of systemic Salmonella Typhimurium infection, we determined that inflammation in tissues triggers thrombosis within vessels via ligation of C-type lectin-like receptor-2 (CLEC-2) on platelets by podoplanin exposed to the vasculature following breaching of the vessel wall. During infection, mice developed thrombi that persisted for weeks within the liver. Bacteria triggered but did not maintain this process, as thrombosis peaked at times when bacteremia was absent and bacteria in tissues were reduced by more than 90% from their peak levels. Thrombus development was triggered by an innate, TLR4-dependent inflammatory cascade that was independent of classical glycoprotein VI-mediated (GPVI-mediated) platelet activation. After infection, IFN-γ release enhanced the number of podoplanin-expressing monocytes and Kupffer cells in the hepatic parenchyma and perivascular sites and absence of TLR4, IFN-γ, or depletion of monocytic-lineage cells or CLEC-2 on platelets markedly inhibited the process. Together, our data indicate that infection-driven thrombosis follows local inflammation and upregulation of podoplanin and platelet activation. The identification of this pathway offers potential therapeutic opportunities to control the devastating consequences of infection-driven thrombosis without increasing the risk of bleeding., Introduction Thrombosis-associated events are among the leading causes of death worldwide. Systemic infections caused by a plethora of bacterial genera can initiate thrombus development. While the mechanisms that underlie this [...]

Published
2015
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12. Concurrent OX40 and CD30 Ligand Blockade Abrogates the CD4-Driven Autoimmunity Associated with CTLA4 and PD1 Blockade while Preserving Excellent Anti-CD8 Tumor Immunity

Author

Nawaf, Maher G., Ulvmar, Maria H., Withers, David R., McConnell, Fiona M., Gaspal, Fabrina M., Webb, Gwilym J., Jones, Nick D., Yagita, Hideo, Allison, James P., and Lane, Peter J. L.

Subjects
CD4-Positive T-Lymphocytes, Mice, Knockout, Programmed Cell Death 1 Receptor, Immunology in the medical area, Autoimmunity, Forkhead Transcription Factors, chemical and pharmacologic phenomena, CD8-Positive T-Lymphocytes, Receptors, OX40, Ligands, Lymphocyte Activation, T-Lymphocytes, Regulatory, Mice, Neoplasms, Immunologi inom det medicinska området, Animals, CTLA-4 Antigen, Immunotherapy, CD30 Ligand, Immunotherapy and Vaccines
Abstract

Although strategies that block FOXP3-dependent regulatory T cell function (CTLA4 blockade) and the inhibitory receptor PD1 have shown great promise in promoting antitumor immune responses in humans, their widespread implementation for cancer immunotherapy has been hampered by significant off-target autoimmune side effects that can be lethal. Our work has shown that absence of OX40 and CD30 costimulatory signals prevents CD4 T cell-driven autoimmunity in Foxp3-deficient mice, suggesting a novel way to block these side effects. In this study, we show that excellent antitumor CD8 T cell responses can be achieved in Foxp3(KO) mice deficient in OX40 and CD30 signals, particularly in the presence of concurrent PD1 blockade. Furthermore, excellent antitumor immune responses can also be achieved using combinations of Abs that block CTLA4, PD1, OX40, and CD30 ligands, without CD4 T cell-driven autoimmunity. By dissociating autoimmune side effects from anticancer immune responses, this potentially shifts this antitumor approach to patients with far less advanced disease.

Published
2017

13. Concurrent OX40 and CD30 Ligand Blockade Abrogates the CD4-Driven Autoimmunity Associated with CTLA4 and PD1 Blockade while Preserving Excellent Anti-CD8 Tumor Immunity

Author

Nawaf, Maher G., primary, Ulvmar, Maria H., additional, Withers, David R., additional, McConnell, Fiona M., additional, Gaspal, Fabrina M., additional, Webb, Gwilym J., additional, Jones, Nick D., additional, Yagita, Hideo, additional, Allison, James P., additional, and Lane, Peter J. L., additional

Published
2017
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14. Resolving Salmonella infection reveals dynamic and persisting changes in murine bone marrow progenitor cell phenotype and function

Author

Ross, Ewan A., Flores-Langarica, Adriana, Bobat, Saeeda, Coughlan, Ruth E., Marshall, Jennifer L., Hitchcock, Jessica R., Cook, Charlotte N., Carvalho-Gaspar, Manuela M., Mitchell, Andrea M., Clarke, Mary, Garcia, Paloma, Cobbold, Mark, Mitchell, Tim J., Henderson, Ian R., Jones, Nick D., Anderson, Graham, Buckley, Christopher D., and Cunningham, Adam F.

Abstract

The generation of immune cells from BM precursors is a carefully regulated process. This is essential to limit the potential for oncogenesis and autoimmunity yet protect against infection. How infection modulates this is unclear. Salmonella can colonize systemic sites including the BM and spleen. This resolving infection has multiple IFN-γ-mediated acute and chronic effects on BM progenitors, and during the first week of infection IFN-γ is produced by myeloid, NK, NKT, CD4+ T cells, and some lineage-negative cells. After infection, the phenotype of BM progenitors rapidly but reversibly alters, with a peak ∼30-fold increase in Sca-1hi progenitors and a corresponding loss of Sca-1lo/int subsets. Most strikingly, the capacity of donor Sca-1hi cells to reconstitute an irradiated host is reduced; the longer donor mice are exposed to infection, and Sca-1hic-kitint cells have an increased potential to generate B1a-like cells. Thus, Salmonella can have a prolonged influence on BM progenitor functionality not directly related to bacterial persistence. These results reflect changes observed in leucopoiesis during aging and suggest that BM functionality can be modulated by life-long, periodic exposure to infection. Better understanding of this process could offer novel therapeutic opportunities to modulate BM functionality and promote healthy aging.

Published
2014

16. Inflammation-induced formation of fat-associated lymphoid clusters

Author

Bénézech, Cécile, primary, Luu, Nguyet-Thin, additional, Walker, Jennifer A, additional, Kruglov, Andrei A, additional, Loo, Yunhua, additional, Nakamura, Kyoko, additional, Zhang, Yang, additional, Nayar, Saba, additional, Jones, Lucy H, additional, Flores-Langarica, Adriana, additional, McIntosh, Alistair, additional, Marshall, Jennifer, additional, Barone, Francesca, additional, Besra, Gurdyal, additional, Miles, Katherine, additional, Allen, Judith E, additional, Gray, Mohini, additional, Kollias, George, additional, Cunningham, Adam F, additional, Withers, David R, additional, Toellner, Kai Michael, additional, Jones, Nick D, additional, Veldhoen, Marc, additional, Nedospasov, Sergei A, additional, McKenzie, Andrew N J, additional, and Caamaño, Jorge H, additional

Published
2015
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17. ResolvingSalmonellainfection reveals dynamic and persisting changes in murine bone marrow progenitor cell phenotype and function

Author

Ross, Ewan A., primary, Flores-Langarica, Adriana, additional, Bobat, Saeeda, additional, Coughlan, Ruth E., additional, Marshall, Jennifer L., additional, Hitchcock, Jessica R., additional, Cook, Charlotte N., additional, Carvalho-Gaspar, Manuela M., additional, Mitchell, Andrea M., additional, Clarke, Mary, additional, Garcia, Paloma, additional, Cobbold, Mark, additional, Mitchell, Tim J., additional, Henderson, Ian R., additional, Jones, Nick D., additional, Anderson, Graham, additional, Buckley, Christopher D., additional, and Cunningham, Adam F., additional

Published
2014
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45. THE VISUALIZATION OF T CELL RESPONSES1

Author

Barbara, Jeffrey A.J., primary, Gilot, Bryant J., additional, Hara, Masaki, additional, Van Maurik, Andre, additional, Jones, Nick D., additional, Turvey, Stuart E., additional, and Wood, Kathryn J., additional

Published
1999
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