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168 results on '"Udalova, Irina A."'

1. Single cell spatial analysis reveals inflammatory foci of immature neutrophil and CD8 T cells in COVID-19 lungs

Author

Weeratunga, Praveen, Denney, Laura, Bull, Joshua A., Repapi, Emmanouela, Sergeant, Martin, Etherington, Rachel, Vuppussetty, Chaitanya, Turner, Gareth D. H., Clelland, Colin, Woo, Jeongmin, Cross, Amy, Issa, Fadi, de Andrea, Carlos Eduardo, Melero Bermejo, Ignacio, Sims, David, McGowan, Simon, Zurke, Yasemin-Xiomara, Ahern, David J., Gamez, Eddie C., Whalley, Justin, Richards, Duncan, Klenerman, Paul, Monaco, Claudia, Udalova, Irina A., Dong, Tao, Antanaviciute, Agne, Ogg, Graham, Knight, Julian C., Byrne, Helen M., Taylor, Stephen, and Ho, Ling-Pei

Published
2023
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4. Constructing custom-made radiotranscriptomic signatures of vascular inflammation from routine CT angiograms: a prospective outcomes validation study in COVID-19

Author

Ahern, David J, Ai, Zhichao, Ainsworth, Mark, Allan, Chris, Allcock, Alice, Angus, Brian, Ansari, M Azim, Arancibia-Cárcamo, Carolina, Aschenbrenner, Dominik, Attar, Moustafa, Baillie, J Kenneth, Barnes, Eleanor, Bashford-Rogers, Rachael, Bashyal, Archana, Beer, Sally, Berridge, Georgina, Beveridge, Amy, Bibi, Sagida, Bicanic, Tihana, Blackwell, Luke, Bowness, Paul, Brent, Andrew, Brown, Andrew, Broxholme, John, Buck, David, Burnham, Katie, Byrne, Helen, Camara, Susana, Ferreira, Ivan Candido, Charles, Philip, Chen, Wentao, Chen, Yi-Ling, Chong, Amanda, Clutterbuck, Elizabeth, Coles, Mark, Conlon, Christopher, Cornall, Richard, Cribbs, Adam, Curion, Fabiola, Davenport, Emma, Davidson, Neil, Davis, Simon, Dendrou, Calliope, Dequaire, Julie, Dib, Lea, Docker, James, Dold, Christina, Dong, Tao, Downes, Damien, Drakesmith, Hal, Dunachie, Susanna, Duncan, David, Eijsbouts, Chris, Esnouf, Robert, Espinosa, Alexis, Etherington, Rachel, Fairfax, Benjamin, Fairhead, Rory, Fang, Hai, Fassih, Shayan, Felle, Sally, Fernandez Mendoza, Maria, Ferreira, Ricardo, Fischer, Roman, Foord, Thomas, Forrow, Aden, Frater, John, Fries, Anastasia, Gallardo Sanchez, Veronica, Garner, Lucy, Geeves, Clementine, Georgiou, Dominique, Godfrey, Leila, Golubchik, Tanya, Gomez Vazquez, Maria, Green, Angie, Harper, Hong, Harrington, Heather, Heilig, Raphael, Hester, Svenja, Hill, Jennifer, Hinds, Charles, Hird, Clare, Ho, Ling-Pei, Hoekzema, Renee, Hollis, Benjamin, Hughes, Jim, Hutton, Paula, Jackson-Wood, Matthew, Jainarayanan, Ashwin, James-Bott, Anna, Jansen, Kathrin, Jeffery, Katie, Jones, Elizabeth, Jostins, Luke, Kerr, Georgina, Kim, David, Klenerman, Paul, Knight, Julian, Kumar, Vinod, Kumar Sharma, Piyush, Kurupati, Prathiba, Kwok, Andrew, Lee, Angela, Linder, Aline, Lockett, Teresa, Lonie, Lorne, Lopopolo, Maria, Lukoseviciute, Martyna, Luo, Jian, Marinou, Spyridoula, Marsden, Brian, Martinez, Jose, Matthews, Philippa, Mazurczyk, Michalina, McGowan, Simon, McKechnie, Stuart, Mead, Adam, Mentzer, Alexander, Mi, Yuxin, Monaco, Claudia, Montadon, Ruddy, Napolitani, Giorgio, Nassiri, Isar, Novak, Alex, O'Brien, Darragh, O'Connor, Daniel, O'Donnell, Denise, Ogg, Graham, Overend, Lauren, Park, Inhye, Pavord, Ian, Peng, Yanchun, Penkava, Frank, Pereira Pinho, Mariana, Perez, Elena, Pollard, Andrew, Powrie, Fiona, Psaila, Bethan, Quan, T Phuong, Repapi, Emmanouela, Revale, Santiago, Silva-Reyes, Laura, Richard, Jean-Baptiste, Rich-Griffin, Charlotte, Ritter, Thomas, Rollier, Christine, Rowland, Matthew, Ruehle, Fabian, Salio, Mariolina, Sansom, Stephen Nicholas, Sanches Peres, Raphael, Santos Delgado, Alberto, Sauka-Spengler, Tatjana, Schwessinger, Ron, Scozzafava, Giuseppe, Screaton, Gavin, Seigal, Anna, Semple, Malcolm, Sergeant, Martin, Simoglou Karali, Christina, Sims, David, Skelly, Donal, Slawinski, Hubert, Sobrinodiaz, Alberto, Sousos, Nikolaos, Stafford, Lizzie, Stockdale, Lisa, Strickland, Marie, Sumray, Otto, Sun, Bo, Taylor, Chelsea, Taylor, Stephen, Taylor, Adan, Thongjuea, Supat, Thraves, Hannah, Todd, John, Tomic, Adriana, Tong, Orion, Trebes, Amy, Trzupek, Dominik, Tucci, Felicia Anna, Turtle, Lance, Udalova, Irina, Uhlig, Holm, van Grinsven, Erinke, Vendrell, Iolanda, Verheul, Marije, Voda, Alexandru, Wang, Guanlin, Wang, Lihui, Wang, Dapeng, Watkinson, Peter, Watson, Robert, Weinberger, Michael, Whalley, Justin, Witty, Lorna, Wray, Katherine, Xue, Luzheng, Yuen Yeung, Hing, Yin, Zixi, Young, Rebecca, Youngs, Jonathan, Zhang, Ping, Zurke, Yasemin-Xiomara, Banning, Adrian, Antonopoulos, Alexios, Bajaj, Amrita, Kelion, Andrew, Deshpande, Aparna, Kardos, Attila, Hudson, Benjamin, Koo, Bon-Kwon, Shirodaria, Cheerag, Xie, Cheng, Kotanidis, Christos, Mahon, Ciara, Berry, Colin, Adlam, David, Newby, David, Connolly, Derek, Scaletta, Diane, Alexander, Donna, Nicol, Ed, McAlindon, Elisa, Oikonomou, Evangelos, Pugliese, Francesca, Pontone, Gianluca, Benedetti, Giulia, He, Guo-Wei, West, Henry, Kondo, Hidekazu, Benedek, Imre, Das, Intrajeet, Deanfield, John, Graby, John, Greenwood, John, Rodrigues, Jonathan, Ge, Junbo, Channon, Keith, Fabritz, Larissa, Fan, Li-Juan, Kingham, Lucy, Guglielmo, Marco, Lyasheva, Maria, Schmitt, Matthias, Beer, Meinrad, Anderson, Michelle, Desai, Milind, Marwan, Mohamed, Takahashi, Naohiko, Mehta, Nehal, Dai, Neng, Screaton, Nicholas, Sabharwal, Nikant, Maurovich-Horvat, Pál, Rao, Praveen, Kotronias, Rafail, Kharbanda, Rajesh, Preston, Rebecca, Wood, Richard, Blankstein, Ron, Rajani, Ronak, Mirsadraee, Saeed, Munir, Shahzad, Thomas, Sheena, Neubauer, Stefan, Klömpken, Steffen, Petersen, Steffen, Achenbach, Stephan, Anthony, Susan, Mak, Sze, Mittal, Tarun, Benedek, Theodora, Sharma, Vinoda, Lin, Wen-Hua, Kotanidis, Christos P, Rodrigues, Jonathan C L, O’Connor, Daniel, Siddique, Muhammad, Lockstone, Helen, Oikonomou, Evangelos K, Badi, Ileana, Lumley, Sheila F, Constantinides, Bede, Sanderson, Nicholas, Rodger, Gillian, Chau, Kevin K, Lodge, Archie, Tsakok, Maria, Gleeson, Fergus, Indrajeet, Das, Hudson, Benjamin J, Srivastava, Vivek, Farid, Shakil, Krasopoulos, George, Sayeed, Rana, Newby, David E, Channon, Keith M, and Antoniades, Charalambos

Published
2022
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9. Digital transformations in education: Augmented reality in the classroom.

Author

Arkhipova, Maria V., Shutova, Natalia V., Orlova, Olga A., Zhernovaya, Oksana R., Zintsova, Yulia N., and Udalova, Irina M.

Subjects
DIGITAL transformation, EDUCATIONAL planning, DIGITAL technology, EDUCATIONAL technology, AUGMENTED reality, COMPUTER assisted language instruction, DIGITAL natives, EDUCATIONAL change
Abstract

Technology brings significant changes to education, giving teachers opportunities to introduce new educational methods and strategies and build immersive learning experiences important for achieving success in the digital world. Augmented reality is an innovative educational tool, presenting information in a new way that appeals to the modern generation of digital native learners. The article evaluates the impact of augmented reality technology on motivation to learn a foreign language by higher University students. Motivation is the key to successful language learning that stimulates learners to realize their academic potential. The experiment reveals that augmented reality motivates students to learn better, influences their engagement and performance, and boosts learning indicators. This new-age technology, meeting the needs and interests of present-day generation, has a positive impact of students' attention, emotions, self-assurance and belief in academic achievement, promotes a better teacher-student understanding, and therefore opens a new dimension in education. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Distinct synovial tissue macrophage subsets regulate inflammation and remission in rheumatoid arthritis

Author

Alivernini, Stefano, MacDonald, Lucy, Elmesmari, Aziza, Finlay, Samuel, Tolusso, Barbara, Gigante, Maria Rita, Petricca, Luca, Di Mario, Clara, Bui, Laura, Perniola, Simone, Attar, Moustafa, Gessi, Marco, Fedele, Anna Laura, Chilaka, Sabarinadh, Somma, Domenico, Sansom, Stephen N., Filer, Andrew, McSharry, Charles, Millar, Neal L., Kirschner, Kristina, Nerviani, Alessandra, Lewis, Myles J., Pitzalis, Costantino, Clark, Andrew R., Ferraccioli, Gianfranco, Udalova, Irina, Buckley, Christopher D., Gremese, Elisa, McInnes, Iain B., Otto, Thomas D., and Kurowska-Stolarska, Mariola

Published
2020
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19. Plasma iron controls neutrophil production and function

Author

Frost, Joe N., primary, Wideman, Sarah K., additional, Preston, Alexandra E., additional, Teh, Megan R., additional, Ai, Zhichao, additional, Wang, Lihui, additional, Cross, Amy, additional, White, Natasha, additional, Yazicioglu, Yavuz, additional, Bonadonna, Michael, additional, Clarke, Alexander J., additional, Armitage, Andrew E., additional, Galy, Bruno, additional, Udalova, Irina A., additional, and Drakesmith, Hal, additional

Published
2022
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20. Constructing custom-made radiotranscriptomic signatures of vascular inflammation from routine CT angiograms: a prospective outcomes validation study in COVID-19

Author

Kotanidis, Christos P, primary, Xie, Cheng, additional, Alexander, Donna, additional, Rodrigues, Jonathan C L, additional, Burnham, Katie, additional, Mentzer, Alexander, additional, O’Connor, Daniel, additional, Knight, Julian, additional, Siddique, Muhammad, additional, Lockstone, Helen, additional, Thomas, Sheena, additional, Kotronias, Rafail, additional, Oikonomou, Evangelos K, additional, Badi, Ileana, additional, Lyasheva, Maria, additional, Shirodaria, Cheerag, additional, Lumley, Sheila F, additional, Constantinides, Bede, additional, Sanderson, Nicholas, additional, Rodger, Gillian, additional, Chau, Kevin K, additional, Lodge, Archie, additional, Tsakok, Maria, additional, Gleeson, Fergus, additional, Adlam, David, additional, Rao, Praveen, additional, Indrajeet, Das, additional, Deshpande, Aparna, additional, Bajaj, Amrita, additional, Hudson, Benjamin J, additional, Srivastava, Vivek, additional, Farid, Shakil, additional, Krasopoulos, George, additional, Sayeed, Rana, additional, Ho, Ling-Pei, additional, Neubauer, Stefan, additional, Newby, David E, additional, Channon, Keith M, additional, Deanfield, John, additional, Antoniades, Charalambos, additional, Ahern, David J, additional, Ai, Zhichao, additional, Ainsworth, Mark, additional, Allan, Chris, additional, Allcock, Alice, additional, Angus, Brian, additional, Ansari, M Azim, additional, Arancibia-Cárcamo, Carolina, additional, Aschenbrenner, Dominik, additional, Attar, Moustafa, additional, Baillie, J Kenneth, additional, Barnes, Eleanor, additional, Bashford-Rogers, Rachael, additional, Bashyal, Archana, additional, Beer, Sally, additional, Berridge, Georgina, additional, Beveridge, Amy, additional, Bibi, Sagida, additional, Bicanic, Tihana, additional, Blackwell, Luke, additional, Bowness, Paul, additional, Brent, Andrew, additional, Brown, Andrew, additional, Broxholme, John, additional, Buck, David, additional, Byrne, Helen, additional, Camara, Susana, additional, Ferreira, Ivan Candido, additional, Charles, Philip, additional, Chen, Wentao, additional, Chen, Yi-Ling, additional, Chong, Amanda, additional, Clutterbuck, Elizabeth, additional, Coles, Mark, additional, Conlon, Christopher, additional, Cornall, Richard, additional, Cribbs, Adam, additional, Curion, Fabiola, additional, Davenport, Emma, additional, Davidson, Neil, additional, Davis, Simon, additional, Dendrou, Calliope, additional, Dequaire, Julie, additional, Dib, Lea, additional, Docker, James, additional, Dold, Christina, additional, Dong, Tao, additional, Downes, Damien, additional, Drakesmith, Hal, additional, Dunachie, Susanna, additional, Duncan, David, additional, Eijsbouts, Chris, additional, Esnouf, Robert, additional, Espinosa, Alexis, additional, Etherington, Rachel, additional, Fairfax, Benjamin, additional, Fairhead, Rory, additional, Fang, Hai, additional, Fassih, Shayan, additional, Felle, Sally, additional, Fernandez Mendoza, Maria, additional, Ferreira, Ricardo, additional, Fischer, Roman, additional, Foord, Thomas, additional, Forrow, Aden, additional, Frater, John, additional, Fries, Anastasia, additional, Gallardo Sanchez, Veronica, additional, Garner, Lucy, additional, Geeves, Clementine, additional, Georgiou, Dominique, additional, Godfrey, Leila, additional, Golubchik, Tanya, additional, Gomez Vazquez, Maria, additional, Green, Angie, additional, Harper, Hong, additional, Harrington, Heather, additional, Heilig, Raphael, additional, Hester, Svenja, additional, Hill, Jennifer, additional, Hinds, Charles, additional, Hird, Clare, additional, Hoekzema, Renee, additional, Hollis, Benjamin, additional, Hughes, Jim, additional, Hutton, Paula, additional, Jackson-Wood, Matthew, additional, Jainarayanan, Ashwin, additional, James-Bott, Anna, additional, Jansen, Kathrin, additional, Jeffery, Katie, additional, Jones, Elizabeth, additional, Jostins, Luke, additional, Kerr, Georgina, additional, Kim, David, additional, Klenerman, Paul, additional, Kumar, Vinod, additional, Kumar Sharma, Piyush, additional, Kurupati, Prathiba, additional, Kwok, Andrew, additional, Lee, Angela, additional, Linder, Aline, additional, Lockett, Teresa, additional, Lonie, Lorne, additional, Lopopolo, Maria, additional, Lukoseviciute, Martyna, additional, Luo, Jian, additional, Marinou, Spyridoula, additional, Marsden, Brian, additional, Martinez, Jose, additional, Matthews, Philippa, additional, Mazurczyk, Michalina, additional, McGowan, Simon, additional, McKechnie, Stuart, additional, Mead, Adam, additional, Mi, Yuxin, additional, Monaco, Claudia, additional, Montadon, Ruddy, additional, Napolitani, Giorgio, additional, Nassiri, Isar, additional, Novak, Alex, additional, O'Brien, Darragh, additional, O'Connor, Daniel, additional, O'Donnell, Denise, additional, Ogg, Graham, additional, Overend, Lauren, additional, Park, Inhye, additional, Pavord, Ian, additional, Peng, Yanchun, additional, Penkava, Frank, additional, Pereira Pinho, Mariana, additional, Perez, Elena, additional, Pollard, Andrew, additional, Powrie, Fiona, additional, Psaila, Bethan, additional, Quan, T Phuong, additional, Repapi, Emmanouela, additional, Revale, Santiago, additional, Silva-Reyes, Laura, additional, Richard, Jean-Baptiste, additional, Rich-Griffin, Charlotte, additional, Ritter, Thomas, additional, Rollier, Christine, additional, Rowland, Matthew, additional, Ruehle, Fabian, additional, Salio, Mariolina, additional, Sansom, Stephen Nicholas, additional, Sanches Peres, Raphael, additional, Santos Delgado, Alberto, additional, Sauka-Spengler, Tatjana, additional, Schwessinger, Ron, additional, Scozzafava, Giuseppe, additional, Screaton, Gavin, additional, Seigal, Anna, additional, Semple, Malcolm, additional, Sergeant, Martin, additional, Simoglou Karali, Christina, additional, Sims, David, additional, Skelly, Donal, additional, Slawinski, Hubert, additional, Sobrinodiaz, Alberto, additional, Sousos, Nikolaos, additional, Stafford, Lizzie, additional, Stockdale, Lisa, additional, Strickland, Marie, additional, Sumray, Otto, additional, Sun, Bo, additional, Taylor, Chelsea, additional, Taylor, Stephen, additional, Taylor, Adan, additional, Thongjuea, Supat, additional, Thraves, Hannah, additional, Todd, John, additional, Tomic, Adriana, additional, Tong, Orion, additional, Trebes, Amy, additional, Trzupek, Dominik, additional, Tucci, Felicia Anna, additional, Turtle, Lance, additional, Udalova, Irina, additional, Uhlig, Holm, additional, van Grinsven, Erinke, additional, Vendrell, Iolanda, additional, Verheul, Marije, additional, Voda, Alexandru, additional, Wang, Guanlin, additional, Wang, Lihui, additional, Wang, Dapeng, additional, Watkinson, Peter, additional, Watson, Robert, additional, Weinberger, Michael, additional, Whalley, Justin, additional, Witty, Lorna, additional, Wray, Katherine, additional, Xue, Luzheng, additional, Yuen Yeung, Hing, additional, Yin, Zixi, additional, Young, Rebecca, additional, Youngs, Jonathan, additional, Zhang, Ping, additional, Zurke, Yasemin-Xiomara, additional, Banning, Adrian, additional, Antonopoulos, Alexios, additional, Kelion, Andrew, additional, Kardos, Attila, additional, Hudson, Benjamin, additional, Koo, Bon-Kwon, additional, Kotanidis, Christos, additional, Mahon, Ciara, additional, Berry, Colin, additional, Newby, David, additional, Connolly, Derek, additional, Scaletta, Diane, additional, Nicol, Ed, additional, McAlindon, Elisa, additional, Oikonomou, Evangelos, additional, Pugliese, Francesca, additional, Pontone, Gianluca, additional, Benedetti, Giulia, additional, He, Guo-Wei, additional, West, Henry, additional, Kondo, Hidekazu, additional, Benedek, Imre, additional, Das, Intrajeet, additional, Graby, John, additional, Greenwood, John, additional, Rodrigues, Jonathan, additional, Ge, Junbo, additional, Channon, Keith, additional, Fabritz, Larissa, additional, Fan, Li-Juan, additional, Kingham, Lucy, additional, Guglielmo, Marco, additional, Schmitt, Matthias, additional, Beer, Meinrad, additional, Anderson, Michelle, additional, Desai, Milind, additional, Marwan, Mohamed, additional, Takahashi, Naohiko, additional, Mehta, Nehal, additional, Dai, Neng, additional, Screaton, Nicholas, additional, Sabharwal, Nikant, additional, Maurovich-Horvat, Pál, additional, Kharbanda, Rajesh, additional, Preston, Rebecca, additional, Wood, Richard, additional, Blankstein, Ron, additional, Rajani, Ronak, additional, Mirsadraee, Saeed, additional, Munir, Shahzad, additional, Klömpken, Steffen, additional, Petersen, Steffen, additional, Achenbach, Stephan, additional, Anthony, Susan, additional, Mak, Sze, additional, Mittal, Tarun, additional, Benedek, Theodora, additional, Sharma, Vinoda, additional, and Lin, Wen-Hua, additional

Published
2022
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21. Unbiased single cell spatial analysis localises inflammatory clusters of immature neutrophils-CD8 T cells to alveolar progenitor cells in fatal COVID-19 lungs

Author

Weeratunga, Praveen, Denney, Laura, Bull, Joshua A., Repapi, Emmanouela, Sergeant, Martin, Etherington, Rachel, Chaitanya Vuppussetty, Turner, Gareth D.H., Clelland, Colin, Cross, Amy, Issa, Fadi, De Andrea, Carlos Eduardo, Bermejo, Ignacio Melero, Sims, David, McGowan, Simon, Yasemin-Xiomara Zurke, Ahern, David J., Gamez, Eddie C, Whalley, Justin, Richards, Duncan, Klenerman, Paul, Monaca, Claudia, Udalova, Irina A., Dong, Tao, Ogg, Graham, Knight, Julian C., Byrne, Helen M., Taylor, Stephen, and Ling-Pei Ho

Subjects
Organising pnemonia, Spatial proteomics, Immune-structural interactions, Multi-Dimensional Viewer (MDV) software, Spatial analysis, Inflammatory network, Severe COVID-19 disease, COVID-19 lung disease, Diffuse alveolar damage, Spatial Omics Oxford Pipeline (SpOOx)
Abstract

Single cell spatial interrogation of the immune-structural interactions in COVID -19 lungs is challenging, mainly because of the marked cellular infiltrate and architecturally distorted microstructure. To address this, we developed a suite of mathematical tools to search for statistically significant co-locations amongst immune and structural cells identified using 37-plex imaging mass cytometry. This unbiased method revealed a cellular map interleaved with an inflammatory network of immature neutrophils, cytotoxic CD8 T cells, megakaryocytes and monocytes co-located with regenerating alveolar progenitors and endothelium. Of note, a highly active cluster of immature neutrophils and cytotoxic CD8 T cells, was found spatially linked with alveolar progenitor cells, and temporally with the diffuse alveolar damage stage. These findings provide new insights into how immune cells interact in the lungs of severe COVID-19 disease. We provide our pipeline Spatial Omics Oxford Pipeline (SpOOx)and visual-analytical tool, Multi-Dimensional Viewer (MDV) software, as a resource for spatial analysis.

Published
2022
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23. Anti-TNF Therapy

Author

Udalova, Irina, primary, Monaco, Claudia, additional, Nanchahal, Jagdeep, additional, and Feldmann, Marc, additional

Published
2017
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24. Neutrophil phenotypes and functions in cancer: A consensus statement

Author

Quail, Daniela F., primary, Amulic, Borko, additional, Aziz, Monowar, additional, Barnes, Betsy J., additional, Eruslanov, Evgeniy, additional, Fridlender, Zvi G., additional, Goodridge, Helen S., additional, Granot, Zvi, additional, Hidalgo, Andrés, additional, Huttenlocher, Anna, additional, Kaplan, Mariana J., additional, Malanchi, Ilaria, additional, Merghoub, Taha, additional, Meylan, Etienne, additional, Mittal, Vivek, additional, Pittet, Mikael J., additional, Rubio-Ponce, Andrea, additional, Udalova, Irina A., additional, van den Berg, Timo K., additional, Wagner, Denisa D., additional, Wang, Ping, additional, Zychlinsky, Arturo, additional, de Visser, Karin E., additional, Egeblad, Mikala, additional, and Kubes, Paul, additional

Published
2022
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26. Irf5 deficiency in macrophages promotes beneficial adipose tissue expansion and insulin sensitivity during obesity

Author

Dalmas, Elise, Toubal, Amine, Alzaid, Fawaz, Blazek, Katrina, Eames, Hayley L., Lebozec, Kristell, Pini, Maria, Hainault, Isabelle, Montastier, Emilie, Denis, Raphael G.P., Ancel, Patricia, Lacombe, Amelie, Ling, Yin, Allatif, Omran, Cruciani-Guglielmacci, Celine, Andre, Sebastien, Viguerie, Nathalie, Poitou, Christine, Stich, Vladimir, Torcivia, Alexandra, Foufelle, Fabienne, Luquet, Serge, Aron-Wisnewsky, Judith, Langin, Dominique, Clement, Karine, Udalova, Irina A., and Venteclef, Nicolas

Subjects
Obesity -- Genetic aspects -- Care and treatment -- Research, Adipose tissues -- Comparative analysis -- Physiological aspects -- Genetic aspects -- Research, Insulin -- Comparative analysis -- Physiological aspects -- Genetic aspects -- Research, Macrophages -- Comparative analysis -- Physiological aspects -- Genetic aspects -- Research, Transcription factors -- Physiological aspects -- Research, Biological sciences, Health
Abstract

Accumulation of visceral adipose tissue correlates with elevated inflammation and increased risk of metabolic diseases. However, little is known about the molecular mechanisms that control its pathological expansion. Transcription factor interferon regulatory factor 5 (IRF5) has been implicated in polarizing macrophages towards an inflammatory phenotype. Here we demonstrate that mice lacking Irf5, when placed on a high-fat diet, show no difference in the growth of their epididymal white adipose tissue (epiWAT) but they show expansion of their subcutaneous white adipose tissue, as compared to wild-type (WT) mice on the same diet. EpiWAT from Irf5-deficient mice is marked by accumulation of alternatively activated macrophages, higher collagen deposition that restricts adipocyte size, and enhanced insulin sensitivity compared to epiWAT from WT mice. In obese individuals, IRF5 expression is negatively associated with insulin sensitivity and collagen deposition in visceral adipose tissue. Genome-wide analysis of gene expression in adipose tissue macrophages highlights the transforming growth factor β1 (TGFB1) gene itself as a direct target of IRF5-mediated inhibition. This study uncovers a new function for IRF5 in controlling the relative mass of different adipose tissue depots and thus insulin sensitivity in obesity, and it suggests that inhibition of IRF5 may promote a healthy metabolic state during this condition., Obesity and its common comorbidities, including glucose intolerance and type 2 diabetes (T2D), are frequently associated with the accumulation of adipose tissue in the intra-abdominal region, (so-called visceral obesity) (1). [...]

Published
2015
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27. Deuterated Arachidonic Acid Ameliorates Lipopolysaccharide-Induced Lung Damage in Mice

Author

Molchanova, Alla Y., primary, Rjabceva, Svetlana N., additional, Melik-Kasumov, Tigran B., additional, Pestov, Nikolay B., additional, Angelova, Plamena R., additional, Shmanai, Vadim V., additional, Sharko, Olga L., additional, Bekish, Andrei V., additional, James, Genevieve, additional, Park, Hui Gyu, additional, Udalova, Irina A., additional, Brenna, J. Thomas, additional, and Shchepinov, Mikhail S., additional

Published
2022
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28. Plasma iron controls neutrophil production and function

Author

Frost, Joe N, primary, Wideman, Sarah K, additional, Preston, Alexandra E, additional, Teh, Megan R, additional, Ai, Zhichao, additional, Wang, Lihui, additional, Cross, Amy, additional, White, Natasha, additional, Yazicioglu, Yavuz, additional, Bonadonna, Michael, additional, Clarke, Alexander, additional, Armitage, Andrew E, additional, Galy, Bruno, additional, Udalova, Irina A, additional, and Drakesmith, Hal, additional

Published
2022
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29. A blood atlas of COVID-19 defines hallmarks of disease severity and specificity

Author

Ahern, David J., primary, Ai, Zhichao, additional, Ainsworth, Mark, additional, Allan, Chris, additional, Allcock, Alice, additional, Angus, Brian, additional, Ansari, M. Azim, additional, Arancibia-Cárcamo, Carolina V., additional, Aschenbrenner, Dominik, additional, Attar, Moustafa, additional, Baillie, J. Kenneth, additional, Barnes, Eleanor, additional, Bashford-Rogers, Rachael, additional, Bashyal, Archana, additional, Beer, Sally, additional, Berridge, Georgina, additional, Beveridge, Amy, additional, Bibi, Sagida, additional, Bicanic, Tihana, additional, Blackwell, Luke, additional, Bowness, Paul, additional, Brent, Andrew, additional, Brown, Andrew, additional, Broxholme, John, additional, Buck, David, additional, Burnham, Katie L., additional, Byrne, Helen, additional, Camara, Susana, additional, Candido Ferreira, Ivan, additional, Charles, Philip, additional, Chen, Wentao, additional, Chen, Yi-Ling, additional, Chong, Amanda, additional, Clutterbuck, Elizabeth A., additional, Coles, Mark, additional, Conlon, Christopher P., additional, Cornall, Richard, additional, Cribbs, Adam P., additional, Curion, Fabiola, additional, Davenport, Emma E., additional, Davidson, Neil, additional, Davis, Simon, additional, Dendrou, Calliope A., additional, Dequaire, Julie, additional, Dib, Lea, additional, Docker, James, additional, Dold, Christina, additional, Dong, Tao, additional, Downes, Damien, additional, Drakesmith, Hal, additional, Dunachie, Susanna J., additional, Duncan, David A., additional, Eijsbouts, Chris, additional, Esnouf, Robert, additional, Espinosa, Alexis, additional, Etherington, Rachel, additional, Fairfax, Benjamin, additional, Fairhead, Rory, additional, Fang, Hai, additional, Fassih, Shayan, additional, Felle, Sally, additional, Fernandez Mendoza, Maria, additional, Ferreira, Ricardo, additional, Fischer, Roman, additional, Foord, Thomas, additional, Forrow, Aden, additional, Frater, John, additional, Fries, Anastasia, additional, Gallardo Sanchez, Veronica, additional, Garner, Lucy C., additional, Geeves, Clementine, additional, Georgiou, Dominique, additional, Godfrey, Leila, additional, Golubchik, Tanya, additional, Gomez Vazquez, Maria, additional, Green, Angie, additional, Harper, Hong, additional, Harrington, Heather A., additional, Heilig, Raphael, additional, Hester, Svenja, additional, Hill, Jennifer, additional, Hinds, Charles, additional, Hird, Clare, additional, Ho, Ling-Pei, additional, Hoekzema, Renee, additional, Hollis, Benjamin, additional, Hughes, Jim, additional, Hutton, Paula, additional, Jackson-Wood, Matthew A., additional, Jainarayanan, Ashwin, additional, James-Bott, Anna, additional, Jansen, Kathrin, additional, Jeffery, Katie, additional, Jones, Elizabeth, additional, Jostins, Luke, additional, Kerr, Georgina, additional, Kim, David, additional, Klenerman, Paul, additional, Knight, Julian C., additional, Kumar, Vinod, additional, Kumar Sharma, Piyush, additional, Kurupati, Prathiba, additional, Kwok, Andrew, additional, Lee, Angela, additional, Linder, Aline, additional, Lockett, Teresa, additional, Lonie, Lorne, additional, Lopopolo, Maria, additional, Lukoseviciute, Martyna, additional, Luo, Jian, additional, Marinou, Spyridoula, additional, Marsden, Brian, additional, Martinez, Jose, additional, Matthews, Philippa C., additional, Mazurczyk, Michalina, additional, McGowan, Simon, additional, McKechnie, Stuart, additional, Mead, Adam, additional, Mentzer, Alexander J., additional, Mi, Yuxin, additional, Monaco, Claudia, additional, Montadon, Ruddy, additional, Napolitani, Giorgio, additional, Nassiri, Isar, additional, Novak, Alex, additional, O'Brien, Darragh P., additional, O'Connor, Daniel, additional, O'Donnell, Denise, additional, Ogg, Graham, additional, Overend, Lauren, additional, Park, Inhye, additional, Pavord, Ian, additional, Peng, Yanchun, additional, Penkava, Frank, additional, Pereira Pinho, Mariana, additional, Perez, Elena, additional, Pollard, Andrew J., additional, Powrie, Fiona, additional, Psaila, Bethan, additional, Quan, T. Phuong, additional, Repapi, Emmanouela, additional, Revale, Santiago, additional, Silva-Reyes, Laura, additional, Richard, Jean-Baptiste, additional, Rich-Griffin, Charlotte, additional, Ritter, Thomas, additional, Rollier, Christine S., additional, Rowland, Matthew, additional, Ruehle, Fabian, additional, Salio, Mariolina, additional, Sansom, Stephen Nicholas, additional, Sanches Peres, Raphael, additional, Santos Delgado, Alberto, additional, Sauka-Spengler, Tatjana, additional, Schwessinger, Ron, additional, Scozzafava, Giuseppe, additional, Screaton, Gavin, additional, Seigal, Anna, additional, Semple, Malcolm G., additional, Sergeant, Martin, additional, Simoglou Karali, Christina, additional, Sims, David, additional, Skelly, Donal, additional, Slawinski, Hubert, additional, Sobrinodiaz, Alberto, additional, Sousos, Nikolaos, additional, Stafford, Lizzie, additional, Stockdale, Lisa, additional, Strickland, Marie, additional, Sumray, Otto, additional, Sun, Bo, additional, Taylor, Chelsea, additional, Taylor, Stephen, additional, Taylor, Adan, additional, Thongjuea, Supat, additional, Thraves, Hannah, additional, Todd, John A., additional, Tomic, Adriana, additional, Tong, Orion, additional, Trebes, Amy, additional, Trzupek, Dominik, additional, Tucci, Felicia Anna, additional, Turtle, Lance, additional, Udalova, Irina, additional, Uhlig, Holm, additional, van Grinsven, Erinke, additional, Vendrell, Iolanda, additional, Verheul, Marije, additional, Voda, Alexandru, additional, Wang, Guanlin, additional, Wang, Lihui, additional, Wang, Dapeng, additional, Watkinson, Peter, additional, Watson, Robert, additional, Weinberger, Michael, additional, Whalley, Justin, additional, Witty, Lorna, additional, Wray, Katherine, additional, Xue, Luzheng, additional, Yeung, Hing Yuen, additional, Yin, Zixi, additional, Young, Rebecca K., additional, Youngs, Jonathan, additional, Zhang, Ping, additional, and Zurke, Yasemin-Xiomara, additional

Published
2022
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30. Interferon regulatory factor-5-dependent CD11c+ macrophages contribute to the formation of rupture–prone atherosclerotic plaques

Author

Edsfeldt, Andreas, primary, Swart, Maarten, additional, Singh, Pratibha, additional, Dib, Lea, additional, Sun, Jiangming, additional, Cole, Jennifer E, additional, Park, Inhye, additional, Al-Sharify, Dania, additional, Persson, Ana, additional, Nitulescu, Mihaela, additional, Borges, Patricia Das Neves, additional, Kassiteridi, Christina, additional, Goddard, Michael E, additional, Lee, Regent, additional, Volkov, Petr, additional, Orho-Melander, Marju, additional, Maegdefessel, Lars, additional, Nilsson, Jan, additional, Udalova, Irina, additional, Goncalves, Isabel, additional, and Monaco, Claudia, additional

Published
2022
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33. Hyperglycemia Induces Trained Immunity in Macrophages and Their Precursors and Promotes Atherosclerosis

Author

Edgar, Laurienne, primary, Akbar, Naveed, additional, Braithwaite, Adam T., additional, Krausgruber, Thomas, additional, Gallart-Ayala, Héctor, additional, Bailey, Jade, additional, Corbin, Alastair L., additional, Khoyratty, Tariq E., additional, Chai, Joshua T., additional, Alkhalil, Mohammad, additional, Rendeiro, André F., additional, Ziberna, Klemen, additional, Arya, Ritu, additional, Cahill, Thomas J., additional, Bock, Christoph, additional, Laurencikiene, Jurga, additional, Crabtree, Mark J., additional, Lemieux, Madeleine E., additional, Riksen, Niels P., additional, Netea, Mihai G., additional, Wheelock, Craig E., additional, Channon, Keith M., additional, Rydén, Mikael, additional, Udalova, Irina A., additional, Carnicer, Ricardo, additional, and Choudhury, Robin P., additional

Published
2021
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34. The Zinc Finger Protein Zbtb18 Represses Expression of Class I Phosphatidylinositol 3-Kinase Subunits and Inhibits Plasma Cell Differentiation

Author

Xie, Bin, primary, Khoyratty, Tariq E., additional, Abu-Shah, Enas, additional, F. Cespedes, Pablo, additional, MacLean, Andrew J., additional, Pirgova, Gabriela, additional, Hu, Zhiyuan, additional, Ahmed, Ahmed A., additional, Dustin, Michael L., additional, Udalova, Irina A., additional, and Arnon, Tal I., additional

Published
2021
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35. IRF5 promotes influenza-induced inflammatory responses in human iPSC-derived myeloid cells and murine models

Author

Forbester, Jessica L, Clement, Mathew, Wellington, Dannielle, Yeung, Amy, Dimonte, Sandra, Marsden, Morgan, Chapman, Lucy, Coomber, Eve L, Tolley, Charlotte, Lees, Emily, Hale, Christine, Clare, Simon, Udalova, Irina, Dong, Tao, Dougan, Gordon, Humphreys, Ian R, Tolley, Charlotte [0000-0002-1119-7983], Dougan, Gordon [0000-0003-0022-965X], and Apollo - University of Cambridge Repository

Subjects
Macrophages, Induced Pluripotent Stem Cells, iPSCs, Adaptive Immunity, Virus Replication, Immunity, Innate, Disease Models, Animal, Mice, Orthomyxoviridae Infections, inflammation, Influenza A virus, IRF5, Host-Pathogen Interactions, Influenza, Human, Interferon Regulatory Factors, Interferon Type I, Animals, Humans, dendritic cells, influenza, Lung
Abstract

Recognition of Influenza A virus (IAV) by the innate immune system triggers pathways that restrict viral replication, activates innate immune cells, and regulates adaptive immunity. However, excessive innate immune activation can exaggerate disease. The pathways promoting excessive activation are incompletely understood, with limited experimental models to investigate mechanisms driving influenza-induced inflammation in humans. Interferon regulatory factor (IRF5) is a transcription factor that plays important roles in induction of cytokines after viral sensing. In an in vivo model of IAV infection, IRF5 deficiency reduced IAV-driven immune pathology and associated inflammatory cytokine production, specifically reducing cytokine-producing myeloid cell populations in Irf5 -/- mice, but not impacting type 1 IFN production or virus replication. Using cytometry by time-of-flight (CyTOF), we identified that human lung IRF5 expression was highest in cells of the myeloid lineage. To investigate the role of IRF5 in mediating human inflammatory responses by myeloid cells to IAV, we employed human induced pluripotent stem cells (hIPSCs) with biallelic mutations in IRF5, demonstrating for the first time iPS-derived dendritic cells (iPS-DCs) with biallelic mutations can be used to investigate regulation of human virus-induced immune responses. Using this technology, we reveal that IRF5 deficiency in human DCs, or macrophages, corresponded with reduced virus-induced inflammatory cytokine production, with IRF5 acting downstream of TLR7 and, possibly, RIG-I after viral sensing. Thus, IRF5 acts as a regulator of myeloid cell inflammatory cytokine production during IAV infection in mice and humans, and drives immune-mediated viral pathogenesis independently of type 1 IFN and virus replication.ImportanceThe inflammatory response to Influenza A virus (IAV) participates in infection control but contributes to disease severity. After viral detection intracellular pathways are activated, initiating cytokine production, but these pathways are incompletely understood. We show that interferon regulatory factor 5 (IRF5) mediates IAV-induced inflammation and, in mice, drives pathology. This was independent of antiviral type 1 IFN and virus replication, implying that IRF5 could be specifically targeted to treat influenza-induced inflammation. We show for the first time that human iPSC technology can be exploited in genetic studies of virus-induced immune responses. Using this technology, we deleted IRF5 in human myeloid cells. These IRF5-deficient cells exhibited impaired influenza-induced cytokine production and revealed that IRF5 acts downstream of Toll-like receptor 7 and possibly retinoic acid-inducible gene-I. Our data demonstrate the importance of IRF5 in influenza-induced inflammation, suggesting genetic variation in the IRF5 gene may influence host susceptibility to viral diseases.

Published
2020

36. Воспоминания Надежды Моллер – ценный источник для исследования биографии Н.Я. Бичурина

Author

Udalova Irina Vitalevna

Subjects
воспоминания, Моллер, Бичурин, биографистика
Abstract

В статье рассмотрены воспоминания внучатой племянницы Н.Я. Бичурина писательницы Н.С. Моллер в качестве источника для изучения биографии ученого, его характера и мировоззрения, влияния на их формирование конкретных фактов и обстоятельств китайского, петербургского и других периодов его жизни. Эти воспоминания были использованы в научной литературе и в документально-художественных произведениях.

Published
2020

37. ENDOTHELIAL CELL-DERIVED EXTRACELLULAR VESICLES ELICIT NEUTROPHIL DEPLOYMENT FROM THE SPLEEN FOLLOWING ACUTE MYOCARDIAL INFARCTION

Author

Akbar, Naveed, primary, Braithwaite, Adam, additional, Corr, Emma, additional, Koelwyn, Graeme, additional, van Solingen, Coen, additional, Cochain, Clement, additional, Saliba, Antoine-Emmanuel, additional, Corbin, Alastair, additional, Pezzolla, Daniela, additional, Edgar, Laurienne, additional, Gunadasa-Rohling, Mala, additional, Banerjee, Abhirup, additional, Paget, Daan, additional, Lee, Charlotte, additional, Hogg, Eleanor, additional, Costin, Adam, additional, Dhaliwal, Raman, additional, Johnson, Errin, additional, Krausgruber, Thomas, additional, Riepsaame, Joey, additional, Melling, Genevieve, additional, Shanmuganathan, Mayooran, additional, Acute Myocardial Infarction Study, Oxford, additional, Bock, Christoph, additional, Carter, David, additional, Channon, Keith, additional, Riley, Paul, additional, Udalova, Irina, additional, Moore, Kathryn, additional, Anthony, Daniel, additional, and Choudhury, Robin, additional

Published
2020
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38. Co-option of Neutrophil Fates by Tissue Environments

Author

Ballesteros, Iván, primary, Rubio-Ponce, Andrea, additional, Genua, Marco, additional, Lusito, Eleonora, additional, Kwok, Immanuel, additional, Fernández-Calvo, Gabriel, additional, Khoyratty, Tariq E., additional, van Grinsven, Erinke, additional, González-Hernández, Sara, additional, Nicolás-Ávila, José Ángel, additional, Vicanolo, Tommaso, additional, Maccataio, Antonio, additional, Benguría, Alberto, additional, Li, Jackson LiangYao, additional, Adrover, José M., additional, Aroca-Crevillen, Alejandra, additional, Quintana, Juan A., additional, Martín-Salamanca, Sandra, additional, Mayo, Francisco, additional, Ascher, Stefanie, additional, Barbiera, Giulia, additional, Soehnlein, Oliver, additional, Gunzer, Matthias, additional, Ginhoux, Florent, additional, Sánchez-Cabo, Fátima, additional, Nistal-Villán, Estanislao, additional, Schulz, Christian, additional, Dopazo, Ana, additional, Reinhardt, Christoph, additional, Udalova, Irina A., additional, Ng, Lai Guan, additional, Ostuni, Renato, additional, and Hidalgo, Andrés, additional

Published
2020
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39. ROS-producing immature neutrophils in giant cell arteritis are linked to vascular pathologies

Author

Wang, Lihui, primary, Ai, Zhichao, additional, Khoyratty, Tariq, additional, Zec, Kristina, additional, Eames, Hayley L., additional, van Grinsven, Erinke, additional, Hudak, Alison, additional, Morris, Susan, additional, Ahern, David, additional, Monaco, Claudia, additional, Eruslanov, Evgeniy B., additional, Luqmani, Raashid, additional, and Udalova, Irina A., additional

Published
2020
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40. Synovial single-cell heterogeneity, zonation and interactions: a patchwork of effectors in arthritis.

Author

Schonfeldova, Barbora, Zec, Kristina, and Udalova, Irina A

Subjects
ENDOTHELIAL cells, SYNOVIAL membranes, NEURONS, INFLAMMATION, CELLULAR signal transduction, RHEUMATOID arthritis, GENE expression profiling, ARTHRITIS
Abstract

Despite extensive research, there is still no treatment that would lead to remission in all patients with rheumatoid arthritis as our understanding of the affected site, the synovium, is still incomplete. Recently, single-cell technologies helped to decipher the cellular heterogeneity of the synovium; however, certain synovial cell populations, such as endothelial cells or peripheral neurons, remain to be profiled on a single-cell level. Furthermore, associations between certain cellular states and inflammation were found; whether these cells cause the inflammation remains to be answered. Similarly, cellular zonation and interactions between individual effectors in the synovium are yet to be fully determined. A deeper understanding of cell signalling and interactions in the synovium is crucial for a better design of therapeutics with the goal of complete remission in all patients. [ABSTRACT FROM AUTHOR]

Published
2022
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41. PYK2 controls intestinal inflammation via activation of IRF5 in macrophages

Author

Ryzhakov, Grigory, primary, Almuttaqi, Hannah, additional, Corbin, Alastair L., additional, Khoyratty, Tariq, additional, Berthold, Dorothee, additional, Bullers, Samuel, additional, Eames, Hayley L, additional, Ai, Zhichao, additional, Bonham, Sarah, additional, Fischer, Roman, additional, Jostins-Dean, Luke, additional, Travis, Simon P.L., additional, Kessler, Benedikt M., additional, and Udalova, Irina A., additional

Published
2020
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44. IRF5 Promotes Influenza Virus-Induced Inflammatory Responses in Human Induced Pluripotent Stem Cell-Derived Myeloid Cells and Murine Models

Author

Forbester, Jessica L., primary, Clement, Mathew, additional, Wellington, Dannielle, additional, Yeung, Amy, additional, Dimonte, Sandra, additional, Marsden, Morgan, additional, Chapman, Lucy, additional, Coomber, Eve L., additional, Tolley, Charlotte, additional, Lees, Emily, additional, Hale, Christine, additional, Clare, Simon, additional, Udalova, Irina, additional, Dong, Tao, additional, Dougan, Gordon, additional, and Humphreys, Ian R., additional

Published
2020
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46. Antibody response to homologous epitopes of Epstein-Barr virus, Mycobacterium avium subsp. paratuberculosis and IRF5 in patients with different connective tissue diseases and in mouse model of antigen-induced arthritis

Author

Bo, Marco, primary, Niegowska, Magdalena, additional, Eames, Hayley L., additional, Almuttaqi, Hannah, additional, Arru, Giannina, additional, Erre, Gian Luca, additional, Passiu, Giuseppe, additional, Khoyratty, Tariq E., additional, van Grinsven, Erinke, additional, Udalova, Irina A., additional, and Sechi, Leonardo A., additional

Published
2020
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48. IRF5 governs liver macrophage activation that promotes hepatic fibrosis in mice and humans

Author

Alzaid, Fawaz, Lagadec, Floriane, Albuquerque, Miguel, Ballaire, Raphaëlle, Orliaguet, Lucie, Hainault, Isabelle, Blugeon, Corinne, Lemoine, Sophie, Lehuen, Agnès, Saliba, David G., Udalova, Irina A., Paradis, Valérie, Foufelle, Fabienne, Venteclef, Nicolas, sophie, lemoine, Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), Centre de recherche sur l'Inflammation (CRI (UMR_S_1149 / ERL_8252 / U1149)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Hôpital Beaujon [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut de biologie de l'ENS Paris (IBENS), Département de Biologie - ENS Paris, École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-École normale supérieure - Paris (ENS-PSL), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Laboratoire d'Excellence INFLAMEX [Paris], Université Sorbonne Paris Cité (USPC), and University of Oxford

Subjects
Liver Cirrhosis, Male, 0301 basic medicine, Apoptosis, Inflammation, Biology, Proinflammatory cytokine, Mice, 03 medical and health sciences, Liver disease, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Nonalcoholic fatty liver disease, medicine, Animals, Humans, Macrophage, Myeloid Cells, Transaminases, Mice, Knockout, Macrophages, Bilirubin, General Medicine, Macrophage Activation, medicine.disease, Mice, Inbred C57BL, 030104 developmental biology, medicine.anatomical_structure, Hepatocyte, Interferon Regulatory Factors, Immunology, Hepatocytes, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Female, medicine.symptom, Hepatic fibrosis, IRF5, Research Article
Abstract

International audience; Hepatic fibrosis arises from inflammation in the liver initiated by resident macrophage activation and massive leukocyte accumulation. Hepatic macrophages hold a central position in maintaining homeostasis in the liver and in the pathogenesis of acute and chronic liver injury linked to fibrogenesis. Interferon regulatory factor 5 (IRF5) has recently emerged as an important proinflammatory transcription factor involved in macrophage activation under acute and chronic inflammation. Here, we revealed that IRF5 is significantly induced in liver macrophages from human subjects developing liver fibrosis from nonalcoholic fatty liver disease or hepatitis C virus infection. Furthermore, IRF5 expression positively correlated with clinical markers of liver damage, such as plasma transaminase and bilirubin levels. Interestingly, mice lacking IRF5 in myeloid cells (MKO) were protected from hepatic fibrosis induced by metabolic or toxic stresses. Transcriptional reprogramming of macrophages lacking IRF5 was characterized by immunosuppressive and antiapoptotic properties. Consequently, IRF5 MKO mice respond to hepatocellular stress by promoting hepatocyte survival, leading to complete protection from hepatic fibrogenesis. Our findings reveal a regulatory network, governed by IRF5, that mediates hepatocyte death and liver fibrosis in mice and humans. Therefore, modulating IRF5 function may be an attractive approach to experimental therapeutics in fibroinflammatory liver disease.

Published
2016
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49. IRF5 guides monocytes toward an inflammatory CD11c+ macrophage phenotype and promotes intestinal inflammation.

Author

Corbin, Alastair L., Gomez-Vazquez, Maria, Berthold, Dorothée L., Attar, Moustafa, Arnold, Isabelle C., Powrie, Fiona M., Sansom, Stephen N., and Udalova, Irina A.

Abstract

Targeting overzealous macrophages: Intestinal homeostasis relies on maintenance of a complex set of interactions between intestinal microbiota and the intestinal immune system. Pathogens that colonize the gut invariably disrupt these interactions and promote intestinal inflammation. Here, Corbin et al. have used a mouse pathobiont, Helicobacter hepaticus, that causes inflammation akin to human inflammatory bowel disease (IBD) to study the role of intestinal macrophages in driving inflammation. Using this model, they found the transcription factor IRF5 to be a critical regulator of macrophage inflammatory potential and that deletion of IRF5 rendered mice resistant to H. hepaticus–driven intestinal inflammation. Their studies propose IRF5 and molecules upstream of IRF5 to be potential drug targets in the treatment of human IBD. Mononuclear phagocytes (MNPs) are vital for maintaining intestinal homeostasis but, in response to acute microbial stimulation, can also trigger immunopathology, accelerating recruitment of Ly6Chi monocytes to the gut. The regulators that control monocyte tissue adaptation in the gut remain poorly understood. Interferon regulatory factor 5 (IRF5) is a transcription factor previously shown to play a key role in maintaining the inflammatory phenotype of macrophages. Here, we investigate the impact of IRF5 on the MNP system and physiology of the gut at homeostasis and during inflammation. We demonstrate that IRF5 deficiency has a limited impact on colon physiology at steady state but ameliorates immunopathology during Helicobacter hepaticus–induced colitis. Inhibition of IRF5 activity in MNPs phenocopies global IRF5 deficiency. Using a combination of bone marrow chimera and single-cell RNA-sequencing approaches, we examined the intrinsic role of IRF5 in controlling colonic MNP development. We demonstrate that IRF5 promotes differentiation of Ly6Chi monocytes into CD11c+ macrophages and controls the production of antimicrobial and inflammatory mediators by these cells. Thus, we identify IRF5 as a key transcriptional regulator of the colonic MNP system during intestinal inflammation. [ABSTRACT FROM AUTHOR]

Published
2020
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