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1. Priming and Maintenance of Adaptive Immunity in the Liver

Author

Kawashima, K, Andreata, F, Beccaria, C, Iannacone, M, Kawashima, Keigo, Andreata, Francesco, Beccaria, Cristian Gabriel, Iannacone, Matteo, Kawashima, K, Andreata, F, Beccaria, C, Iannacone, M, Kawashima, Keigo, Andreata, Francesco, Beccaria, Cristian Gabriel, and Iannacone, Matteo

Abstract

The liver’s unique characteristics have a profound impact on the priming and maintenance of adaptive immunity. This review delves into the cellular circuits that regulate adaptive immune responses in the liver, with a specific focus on hepatitis B virus infection as an illustrative example. A key aspect highlighted is the liver’s specialized role in priming CD8+ T cells, leading to a distinct state of immune hyporesponsiveness. Additionally, the influence of the liver’s hemodynamics and anatomical features, particularly during liver fibrosis and cirrhosis, on the differentiation and function of adaptive immune cells is discussed. While the primary emphasis is on CD8+ T cells, recent findings regarding the involvement of B cells and CD4+ T cells in hepatic immunity are also reviewed. Furthermore, we address the challenges ahead and propose integrating cutting-edge techniques, such as spatial biology, and combining mouse models with human sample analyses to gain comprehensive insights into the liver’s adaptive immunity. This understanding could pave the way for novel therapeutic strategies targeting infectious diseases, malignancies, and inflammatory liver conditions like metabolic dysfunction-associated steatohepatitis and autoimmune hepatitis.

Published
2024

2. Response to contamination of isolated mouse Kupffer cells with liver sinusoidal endothelial cells

Author

Iannacone, M, Blériot, C, Andreata, F, Ficht, X, Laura, C, Garcia-Manteiga, J, Uderhardt, S, Ginhoux, F, Iannacone M., Blériot C., Andreata F., Ficht X., Laura C., Garcia-Manteiga J. M., Uderhardt S., Ginhoux F., Iannacone, M, Blériot, C, Andreata, F, Ficht, X, Laura, C, Garcia-Manteiga, J, Uderhardt, S, Ginhoux, F, Iannacone M., Blériot C., Andreata F., Ficht X., Laura C., Garcia-Manteiga J. M., Uderhardt S., and Ginhoux F.

Published
2022

3. Group 1 ILCs regulate T cell-mediated liver immunopathology by controlling local IL-2 availability

Author

Fumagalli, V, Venzin, V, Di Lucia, P, Moalli, F, Ficht, X, Ambrosi, G, Giustini, L, Andreata, F, Grillo, M, Magini, D, Rava, M, Friedrich, C, Fontenot, J, Bousso, P, Gilmore, S, Khan, S, Baca, M, Vivier, E, Gasteiger, G, Kuka, M, Guidotti, L, Iannacone, M, Fumagalli V., Venzin V., Di Lucia P., Moalli F., Ficht X., Ambrosi G., Giustini L., Andreata F., Grillo M., Magini D., Rava M., Friedrich C., Fontenot J. D., Bousso P., Gilmore S. A., Khan S., Baca M., Vivier E., Gasteiger G., Kuka M., Guidotti L. G., Iannacone M., Fumagalli, V, Venzin, V, Di Lucia, P, Moalli, F, Ficht, X, Ambrosi, G, Giustini, L, Andreata, F, Grillo, M, Magini, D, Rava, M, Friedrich, C, Fontenot, J, Bousso, P, Gilmore, S, Khan, S, Baca, M, Vivier, E, Gasteiger, G, Kuka, M, Guidotti, L, Iannacone, M, Fumagalli V., Venzin V., Di Lucia P., Moalli F., Ficht X., Ambrosi G., Giustini L., Andreata F., Grillo M., Magini D., Rava M., Friedrich C., Fontenot J. D., Bousso P., Gilmore S. A., Khan S., Baca M., Vivier E., Gasteiger G., Kuka M., Guidotti L. G., and Iannacone M.

Abstract

Group 1 innate lymphoid cells (ILCs), which comprise both natural killer (NK) cells and ILC1s, are important innate effectors that can also positively and negatively influence adaptive immune responses. The latter function is generally ascribed to the ability of NK cells to recognize and kill activated T cells. Here, we used multiphoton intravital microscopy in mouse models of hepatitis B to study the intrahepatic behavior of group 1 ILCs and their cross-talk with hepatitis B virus (HBV)-specific CD8+ T cells. We found that hepatocellular antigen recognition by effector CD8+ T cells triggered a prominent increase in the number of hepatic NK cells and ILC1s. Group 1 ILCs colocalized and engaged in prolonged interactions with effector CD8+ T cells undergoing hepatocellular antigen recognition; however, they did not induce T cell apoptosis. Rather, group 1 ILCs constrained CD8+ T cell proliferation by controlling local interleukin-2 (IL-2) availability. Accordingly, group 1 ILC depletion, or genetic removal of their IL-2 receptor a chain, considerably increased the number of intrahepatic HBV-specific effector CD8+ T cells and the attendant immunopathology. Together, these results reveal a role for group 1 ILCs in controlling T cell-mediated liver immunopathology by limiting local IL-2 concentration and have implications for the treatment of chronic HBV infection.

Published
2022

4. AI-SCoRE (artificial intelligence-SARS CoV2 risk evaluation): a fast, objective and fully automated platform to predict the outcome in COVID-19 patients

Author

Palmisano, A, Vignale, D, Boccia, E, Nonis, A, Gnasso, C, Leone, R, Montagna, M, Nicoletti, V, Bianchi, A, Brusamolino, S, Dorizza, A, Moraschini, M, Veettil, R, Cereda, A, Toselli, M, Giannini, F, Loffi, M, Patelli, G, Monello, A, Iannopollo, G, Ippolito, D, Mancini, E, Pontone, G, Vignali, L, Scarnecchia, E, Iannacone, M, Baffoni, L, Sperandio, M, de Carlini, C, Sironi, S, Rapezzi, C, Antiga, L, Jagher, V, Di Serio, C, Furlanello, C, Tacchetti, C, Esposito, A, Palmisano A., Vignale D., Boccia E., Nonis A., Gnasso C., Leone R., Montagna M., Nicoletti V., Bianchi A. G., Brusamolino S., Dorizza A., Moraschini M., Veettil R., Cereda A., Toselli M., Giannini F., Loffi M., Patelli G., Monello A., Iannopollo G., Ippolito D., Mancini E. M., Pontone G., Vignali L., Scarnecchia E., Iannacone M., Baffoni L., Sperandio M., de Carlini C. C., Sironi S., Rapezzi C., Antiga L., Jagher V., Di Serio C., Furlanello C., Tacchetti C., Esposito A., Palmisano, A, Vignale, D, Boccia, E, Nonis, A, Gnasso, C, Leone, R, Montagna, M, Nicoletti, V, Bianchi, A, Brusamolino, S, Dorizza, A, Moraschini, M, Veettil, R, Cereda, A, Toselli, M, Giannini, F, Loffi, M, Patelli, G, Monello, A, Iannopollo, G, Ippolito, D, Mancini, E, Pontone, G, Vignali, L, Scarnecchia, E, Iannacone, M, Baffoni, L, Sperandio, M, de Carlini, C, Sironi, S, Rapezzi, C, Antiga, L, Jagher, V, Di Serio, C, Furlanello, C, Tacchetti, C, Esposito, A, Palmisano A., Vignale D., Boccia E., Nonis A., Gnasso C., Leone R., Montagna M., Nicoletti V., Bianchi A. G., Brusamolino S., Dorizza A., Moraschini M., Veettil R., Cereda A., Toselli M., Giannini F., Loffi M., Patelli G., Monello A., Iannopollo G., Ippolito D., Mancini E. M., Pontone G., Vignali L., Scarnecchia E., Iannacone M., Baffoni L., Sperandio M., de Carlini C. C., Sironi S., Rapezzi C., Antiga L., Jagher V., Di Serio C., Furlanello C., Tacchetti C., and Esposito A.

Abstract

Purpose: To develop and validate an effective and user-friendly AI platform based on a few unbiased clinical variables integrated with advanced CT automatic analysis for COVID-19 patients’ risk stratification. Material and Methods: In total, 1575 consecutive COVID-19 adults admitted to 16 hospitals during wave 1 (February 16-April 29, 2020), submitted to chest CT within 72 h from admission, were retrospectively enrolled. In total, 107 variables were initially collected; 64 extracted from CT. The outcome was survival. A rigorous AI model selection framework was adopted for models selection and automatic CT data extraction. Model performances were compared in terms of AUC. A web–mobile interface was developed using Microsoft PowerApps environment. The platform was externally validated on 213 COVID-19 adults prospectively enrolled during wave 2 (October 14-December 31, 2020). Results: The final cohort included 1125 patients (292 non-survivors, 26%) and 24 variables. Logistic showed the best performance on the complete set of variables (AUC = 0.839 ± 0.009) as in models including a limited set of 13 and 5 variables (AUC = 0.840 ± 0.0093 and AUC = 0.834 ± 0.007). For non-inferior performance, the 5 variables model (age, sex, saturation, well-aerated lung parenchyma and cardiothoracic vascular calcium) was selected as the final model and the extraction of CT-derived parameters was fully automatized. The fully automatic model showed AUC = 0.842 (95% CI: 0.816–0.867) on wave 1 and was used to build a 0–100 scale risk score (AI-SCoRE). The predictive performance was confirmed on wave 2 (AUC 0.808; 95% CI: 0.7402–0.8766). Conclusions: AI-SCoRE is an effective and reliable platform for automatic risk stratification of COVID-19 patients based on a few unbiased clinical data and CT automatic analysis.

Published
2022

5. A subset of Kupffer cells regulates metabolism through the expression of CD36

Author

Bleriot, C, Barreby, E, Dunsmore, G, Ballaire, R, Chakarov, S, Ficht, X, De Simone, G, Andreata, F, Fumagalli, V, Guo, W, Wan, G, Gessain, G, Khalilnezhad, A, Zhang, X, Ang, N, Chen, P, Morgantini, C, Azzimato, V, Kong, W, Liu, Z, Pai, R, Lum, J, Shihui, F, Low, I, Xu, C, Malleret, B, Kairi, M, Balachander, A, Cexus, O, Larbi, A, Lee, B, Newell, E, Ng, L, Phoo, W, Sobota, R, Sharma, A, Howland, S, Chen, J, Bajenoff, M, Yvan-Charvet, L, Venteclef, N, Iannacone, M, Aouadi, M, Ginhoux, F, Bleriot C., Barreby E., Dunsmore G., Ballaire R., Chakarov S., Ficht X., De Simone G., Andreata F., Fumagalli V., Guo W., Wan G., Gessain G., Khalilnezhad A., Zhang X. M., Ang N., Chen P., Morgantini C., Azzimato V., Kong W. T., Liu Z., Pai R., Lum J., Shihui F., Low I., Xu C., Malleret B., Kairi M. F. M., Balachander A., Cexus O., Larbi A., Lee B., Newell E. W., Ng L. G., Phoo W. W., Sobota R. M., Sharma A., Howland S. W., Chen J., Bajenoff M., Yvan-Charvet L., Venteclef N., Iannacone M., Aouadi M., Ginhoux F., Bleriot, C, Barreby, E, Dunsmore, G, Ballaire, R, Chakarov, S, Ficht, X, De Simone, G, Andreata, F, Fumagalli, V, Guo, W, Wan, G, Gessain, G, Khalilnezhad, A, Zhang, X, Ang, N, Chen, P, Morgantini, C, Azzimato, V, Kong, W, Liu, Z, Pai, R, Lum, J, Shihui, F, Low, I, Xu, C, Malleret, B, Kairi, M, Balachander, A, Cexus, O, Larbi, A, Lee, B, Newell, E, Ng, L, Phoo, W, Sobota, R, Sharma, A, Howland, S, Chen, J, Bajenoff, M, Yvan-Charvet, L, Venteclef, N, Iannacone, M, Aouadi, M, Ginhoux, F, Bleriot C., Barreby E., Dunsmore G., Ballaire R., Chakarov S., Ficht X., De Simone G., Andreata F., Fumagalli V., Guo W., Wan G., Gessain G., Khalilnezhad A., Zhang X. M., Ang N., Chen P., Morgantini C., Azzimato V., Kong W. T., Liu Z., Pai R., Lum J., Shihui F., Low I., Xu C., Malleret B., Kairi M. F. M., Balachander A., Cexus O., Larbi A., Lee B., Newell E. W., Ng L. G., Phoo W. W., Sobota R. M., Sharma A., Howland S. W., Chen J., Bajenoff M., Yvan-Charvet L., Venteclef N., Iannacone M., Aouadi M., and Ginhoux F.

Abstract

Tissue macrophages are immune cells whose phenotypes and functions are dictated by origin and niches. However, tissues are complex environments, and macrophage heterogeneity within the same organ has been overlooked so far. Here, we used high-dimensional approaches to characterize macrophage populations in the murine liver. We identified two distinct populations among embryonically derived Kupffer cells (KCs) sharing a core signature while differentially expressing numerous genes and proteins: a major CD206loESAM– population (KC1) and a minor CD206hiESAM+ population (KC2). KC2 expressed genes involved in metabolic processes, including fatty acid metabolism both in steady-state and in diet-induced obesity and hepatic steatosis. Functional characterization by depletion of KC2 or targeted silencing of the fatty acid transporter Cd36 highlighted a crucial contribution of KC2 in the liver oxidative stress associated with obesity. In summary, our study reveals that KCs are more heterogeneous than anticipated, notably describing a subpopulation wired with metabolic functions.

Published
2021

6. Identification of a Kupffer cell subset capable of reverting the T cell dysfunction induced by hepatocellular priming

Author

De Simone, G, Andreata, F, Bleriot, C, Fumagalli, V, Laura, C, Garcia-Manteiga, J, Di Lucia, P, Gilotto, S, Ficht, X, De Ponti, F, Bono, E, Giustini, L, Ambrosi, G, Mainetti, M, Zordan, P, Benechet, A, Rava, M, Chakarov, S, Moalli, F, Bajenoff, M, Guidotti, L, Ginhoux, F, Iannacone, M, De Simone G., Andreata F., Bleriot C., Fumagalli V., Laura C., Garcia-Manteiga J. M., Di Lucia P., Gilotto S., Ficht X., De Ponti F. F., Bono E. B., Giustini L., Ambrosi G., Mainetti M., Zordan P., Benechet A. P., Rava M., Chakarov S., Moalli F., Bajenoff M., Guidotti L. G., Ginhoux F., Iannacone M., De Simone, G, Andreata, F, Bleriot, C, Fumagalli, V, Laura, C, Garcia-Manteiga, J, Di Lucia, P, Gilotto, S, Ficht, X, De Ponti, F, Bono, E, Giustini, L, Ambrosi, G, Mainetti, M, Zordan, P, Benechet, A, Rava, M, Chakarov, S, Moalli, F, Bajenoff, M, Guidotti, L, Ginhoux, F, Iannacone, M, De Simone G., Andreata F., Bleriot C., Fumagalli V., Laura C., Garcia-Manteiga J. M., Di Lucia P., Gilotto S., Ficht X., De Ponti F. F., Bono E. B., Giustini L., Ambrosi G., Mainetti M., Zordan P., Benechet A. P., Rava M., Chakarov S., Moalli F., Bajenoff M., Guidotti L. G., Ginhoux F., and Iannacone M.

Abstract

Kupffer cells (KCs) are highly abundant, intravascular, liver-resident macrophages known for their scavenger and phagocytic functions. KCs can also present antigens to CD8+ T cells and promote either tolerance or effector differentiation, but the mechanisms underlying these discrepant outcomes are poorly understood. Here, we used a mouse model of hepatitis B virus (HBV) infection, in which HBV-specific naive CD8+ T cells recognizing hepatocellular antigens are driven into a state of immune dysfunction, to identify a subset of KCs (referred to as KC2) that cross-presents hepatocellular antigens upon interleukin-2 (IL-2) administration, thus improving the antiviral function of T cells. Removing MHC-I from all KCs, including KC2, or selectively depleting KC2 impaired the capacity of IL-2 to revert the T cell dysfunction induced by intrahepatic priming. In summary, by sensing IL-2 and cross-presenting hepatocellular antigens, KC2 overcome the tolerogenic potential of the hepatic microenvironment, suggesting new strategies for boosting hepatic T cell immunity.

Published
2021

7. Guidelines for the use of flow cytometry and cell sorting in immunological studies (third edition)

Author

Cossarizza, A, Chang, H, Radbruch, A, Abrignani, S, Addo, R, Akdis, M, Andra, I, Andreata, F, Annunziato, F, Arranz, E, Bacher, P, Bari, S, Barnaba, V, Barros-Martins, J, Baumjohann, D, Beccaria, C, Bernardo, D, Boardman, D, Borger, J, Bottcher, C, Brockmann, L, Burns, M, Busch, D, Cameron, G, Cammarata, I, Cassotta, A, Chang, Y, Chirdo, F, Christakou, E, Cicin-Sain, L, Cook, L, Corbett, A, Cornelis, R, Cosmi, L, Davey, M, De Biasi, S, De Simone, G, del Zotto, G, Delacher, M, Di Rosa, F, Santo, J, Diefenbach, A, Dong, J, Dorner, T, Dress, R, Dutertre, C, Eckle, S, Eede, P, Evrard, M, Falk, C, Feuerer, M, Fillatreau, S, Fiz-Lopez, A, Follo, M, Foulds, G, Frobel, J, Gagliani, N, Galletti, G, Gangaev, A, Garbi, N, Garrote, J, Geginat, J, Gherardin, N, Gibellini, L, Ginhoux, F, Godfrey, D, Gruarin, P, Haftmann, C, Hansmann, L, Harpur, C, Hayday, A, Heine, G, Hernandez, D, Herrmann, M, Hoelsken, O, Huang, Q, Huber, S, Huber, J, Huehn, J, Hundemer, M, Hwang, W, Iannacone, M, Ivison, S, Jack, H, Jani, P, Keller, B, Kessler, N, Ketelaars, S, Knop, L, Knopf, J, Koay, H, Kobow, K, Kriegsmann, K, Kristyanto, H, Krueger, A, Kuehne, J, Kunze-Schumacher, H, Kvistborg, P, Kwok, I, Latorre, D, Lenz, D, Levings, M, Lino, A, Liotta, F, Long, H, Lugli, E, Macdonald, K, Maggi, L, Maini, M, Mair, F, Manta, C, Manz, R, Mashreghi, M, Mazzoni, A, Mccluskey, J, Mei, H, Melchers, F, Melzer, S, Mielenz, D, Monin, L, Moretta, L, Multhoff, G, Munoz, L, Munoz-Ruiz, M, Muscate, F, Natalini, A, Neumann, K, Ng, L, Niedobitek, A, Niemz, J, Almeida, L, Notarbartolo, S, Ostendorf, L, Pallett, L, Patel, A, Percin, G, Peruzzi, G, Pinti, M, Pockley, A, Pracht, K, Prinz, I, Pujol-Autonell, I, Pulvirenti, N, Quatrini, L, Quinn, K, Radbruch, H, Rhys, H, Rodrigo, M, Romagnani, C, Saggau, C, Sakaguchi, S, Sallusto, F, Sanderink, L, Sandrock, I, Schauer, C, Scheffold, A, Scherer, H, Schiemann, M, Schildberg, F, Schober, K, Schoen, J, Schuh, W, Schuler, T, Schulz, A, Schulz, S, Schulze, J, Simonetti, S, Singh, J, Sitnik, K, Stark, R, Starossom, S, Stehle, C, Szelinski, F, Tan, L, Tarnok, A, Tornack, J, Tree, T, van Beek, J, van de Veen, W, van Gisbergen, K, Vasco, C, Verheyden, N, von Borstel, A, Ward-Hartstonge, K, Warnatz, K, Waskow, C, Wiedemann, A, Wilharm, A, Wing, J, Wirz, O, Wittner, J, Yang, J, Cossarizza A., Chang H. -D., Radbruch A., Abrignani S., Addo R., Akdis M., Andra I., Andreata F., Annunziato F., Arranz E., Bacher P., Bari S., Barnaba V., Barros-Martins J., Baumjohann D., Beccaria C. G., Bernardo D., Boardman D. A., Borger J., Bottcher C., Brockmann L., Burns M., Busch D. H., Cameron G., Cammarata I., Cassotta A., Chang Y., Chirdo F. G., Christakou E., Cicin-Sain L., Cook L., Corbett A. J., Cornelis R., Cosmi L., Davey M. S., De Biasi S., De Simone G., del Zotto G., Delacher M., Di Rosa F., Santo J. D., Diefenbach A., Dong J., Dorner T., Dress R. J., Dutertre C. -A., Eckle S. B. G., Eede P., Evrard M., Falk C. S., Feuerer M., Fillatreau S., Fiz-Lopez A., Follo M., Foulds G. A., Frobel J., Gagliani N., Galletti G., Gangaev A., Garbi N., Garrote J. A., Geginat J., Gherardin N. A., Gibellini L., Ginhoux F., Godfrey D. I., Gruarin P., Haftmann C., Hansmann L., Harpur C. M., Hayday A. C., Heine G., Hernandez D. C., Herrmann M., Hoelsken O., Huang Q., Huber S., Huber J. E., Huehn J., Hundemer M., Hwang W. Y. K., Iannacone M., Ivison S. M., Jack H. -M., Jani P. K., Keller B., Kessler N., Ketelaars S., Knop L., Knopf J., Koay H. -F., Kobow K., Kriegsmann K., Kristyanto H., Krueger A., Kuehne J. F., Kunze-Schumacher H., Kvistborg P., Kwok I., Latorre D., Lenz D., Levings M. K., Lino A. C., Liotta F., Long H. M., Lugli E., MacDonald K. N., Maggi L., Maini M. K., Mair F., Manta C., Manz R. A., Mashreghi M. -F., Mazzoni A., McCluskey J., Mei H. E., Melchers F., Melzer S., Mielenz D., Monin L., Moretta L., Multhoff G., Munoz L. E., Munoz-Ruiz M., Muscate F., Natalini A., Neumann K., Ng L. G., Niedobitek A., Niemz J., Almeida L. N., Notarbartolo S., Ostendorf L., Pallett L. J., Patel A. A., Percin G. I., Peruzzi G., Pinti M., Pockley A. G., Pracht K., Prinz I., Pujol-Autonell I., Pulvirenti N., Quatrini L., Quinn K. M., Radbruch H., Rhys H., Rodrigo M. B., Romagnani C., Saggau C., Sakaguchi S., Sallusto F., Sanderink L., Sandrock I., Schauer C., Scheffold A., Scherer H. U., Schiemann M., Schildberg F. A., Schober K., Schoen J., Schuh W., Schuler T., Schulz A. R., Schulz S., Schulze J., Simonetti S., Singh J., Sitnik K. M., Stark R., Starossom S., Stehle C., Szelinski F., Tan L., Tarnok A., Tornack J., Tree T. I. M., van Beek J. J. P., van de Veen W., van Gisbergen K., Vasco C., Verheyden N. A., von Borstel A., Ward-Hartstonge K. A., Warnatz K., Waskow C., Wiedemann A., Wilharm A., Wing J., Wirz O., Wittner J., Yang J. H. M., Yang J., Cossarizza, A, Chang, H, Radbruch, A, Abrignani, S, Addo, R, Akdis, M, Andra, I, Andreata, F, Annunziato, F, Arranz, E, Bacher, P, Bari, S, Barnaba, V, Barros-Martins, J, Baumjohann, D, Beccaria, C, Bernardo, D, Boardman, D, Borger, J, Bottcher, C, Brockmann, L, Burns, M, Busch, D, Cameron, G, Cammarata, I, Cassotta, A, Chang, Y, Chirdo, F, Christakou, E, Cicin-Sain, L, Cook, L, Corbett, A, Cornelis, R, Cosmi, L, Davey, M, De Biasi, S, De Simone, G, del Zotto, G, Delacher, M, Di Rosa, F, Santo, J, Diefenbach, A, Dong, J, Dorner, T, Dress, R, Dutertre, C, Eckle, S, Eede, P, Evrard, M, Falk, C, Feuerer, M, Fillatreau, S, Fiz-Lopez, A, Follo, M, Foulds, G, Frobel, J, Gagliani, N, Galletti, G, Gangaev, A, Garbi, N, Garrote, J, Geginat, J, Gherardin, N, Gibellini, L, Ginhoux, F, Godfrey, D, Gruarin, P, Haftmann, C, Hansmann, L, Harpur, C, Hayday, A, Heine, G, Hernandez, D, Herrmann, M, Hoelsken, O, Huang, Q, Huber, S, Huber, J, Huehn, J, Hundemer, M, Hwang, W, Iannacone, M, Ivison, S, Jack, H, Jani, P, Keller, B, Kessler, N, Ketelaars, S, Knop, L, Knopf, J, Koay, H, Kobow, K, Kriegsmann, K, Kristyanto, H, Krueger, A, Kuehne, J, Kunze-Schumacher, H, Kvistborg, P, Kwok, I, Latorre, D, Lenz, D, Levings, M, Lino, A, Liotta, F, Long, H, Lugli, E, Macdonald, K, Maggi, L, Maini, M, Mair, F, Manta, C, Manz, R, Mashreghi, M, Mazzoni, A, Mccluskey, J, Mei, H, Melchers, F, Melzer, S, Mielenz, D, Monin, L, Moretta, L, Multhoff, G, Munoz, L, Munoz-Ruiz, M, Muscate, F, Natalini, A, Neumann, K, Ng, L, Niedobitek, A, Niemz, J, Almeida, L, Notarbartolo, S, Ostendorf, L, Pallett, L, Patel, A, Percin, G, Peruzzi, G, Pinti, M, Pockley, A, Pracht, K, Prinz, I, Pujol-Autonell, I, Pulvirenti, N, Quatrini, L, Quinn, K, Radbruch, H, Rhys, H, Rodrigo, M, Romagnani, C, Saggau, C, Sakaguchi, S, Sallusto, F, Sanderink, L, Sandrock, I, Schauer, C, Scheffold, A, Scherer, H, Schiemann, M, Schildberg, F, Schober, K, Schoen, J, Schuh, W, Schuler, T, Schulz, A, Schulz, S, Schulze, J, Simonetti, S, Singh, J, Sitnik, K, Stark, R, Starossom, S, Stehle, C, Szelinski, F, Tan, L, Tarnok, A, Tornack, J, Tree, T, van Beek, J, van de Veen, W, van Gisbergen, K, Vasco, C, Verheyden, N, von Borstel, A, Ward-Hartstonge, K, Warnatz, K, Waskow, C, Wiedemann, A, Wilharm, A, Wing, J, Wirz, O, Wittner, J, Yang, J, Cossarizza A., Chang H. -D., Radbruch A., Abrignani S., Addo R., Akdis M., Andra I., Andreata F., Annunziato F., Arranz E., Bacher P., Bari S., Barnaba V., Barros-Martins J., Baumjohann D., Beccaria C. G., Bernardo D., Boardman D. A., Borger J., Bottcher C., Brockmann L., Burns M., Busch D. H., Cameron G., Cammarata I., Cassotta A., Chang Y., Chirdo F. G., Christakou E., Cicin-Sain L., Cook L., Corbett A. J., Cornelis R., Cosmi L., Davey M. S., De Biasi S., De Simone G., del Zotto G., Delacher M., Di Rosa F., Santo J. D., Diefenbach A., Dong J., Dorner T., Dress R. J., Dutertre C. -A., Eckle S. B. G., Eede P., Evrard M., Falk C. S., Feuerer M., Fillatreau S., Fiz-Lopez A., Follo M., Foulds G. A., Frobel J., Gagliani N., Galletti G., Gangaev A., Garbi N., Garrote J. A., Geginat J., Gherardin N. A., Gibellini L., Ginhoux F., Godfrey D. I., Gruarin P., Haftmann C., Hansmann L., Harpur C. M., Hayday A. C., Heine G., Hernandez D. C., Herrmann M., Hoelsken O., Huang Q., Huber S., Huber J. E., Huehn J., Hundemer M., Hwang W. Y. K., Iannacone M., Ivison S. M., Jack H. -M., Jani P. K., Keller B., Kessler N., Ketelaars S., Knop L., Knopf J., Koay H. -F., Kobow K., Kriegsmann K., Kristyanto H., Krueger A., Kuehne J. F., Kunze-Schumacher H., Kvistborg P., Kwok I., Latorre D., Lenz D., Levings M. K., Lino A. C., Liotta F., Long H. M., Lugli E., MacDonald K. N., Maggi L., Maini M. K., Mair F., Manta C., Manz R. A., Mashreghi M. -F., Mazzoni A., McCluskey J., Mei H. E., Melchers F., Melzer S., Mielenz D., Monin L., Moretta L., Multhoff G., Munoz L. E., Munoz-Ruiz M., Muscate F., Natalini A., Neumann K., Ng L. G., Niedobitek A., Niemz J., Almeida L. N., Notarbartolo S., Ostendorf L., Pallett L. J., Patel A. A., Percin G. I., Peruzzi G., Pinti M., Pockley A. G., Pracht K., Prinz I., Pujol-Autonell I., Pulvirenti N., Quatrini L., Quinn K. M., Radbruch H., Rhys H., Rodrigo M. B., Romagnani C., Saggau C., Sakaguchi S., Sallusto F., Sanderink L., Sandrock I., Schauer C., Scheffold A., Scherer H. U., Schiemann M., Schildberg F. A., Schober K., Schoen J., Schuh W., Schuler T., Schulz A. R., Schulz S., Schulze J., Simonetti S., Singh J., Sitnik K. M., Stark R., Starossom S., Stehle C., Szelinski F., Tan L., Tarnok A., Tornack J., Tree T. I. M., van Beek J. J. P., van de Veen W., van Gisbergen K., Vasco C., Verheyden N. A., von Borstel A., Ward-Hartstonge K. A., Warnatz K., Waskow C., Wiedemann A., Wilharm A., Wing J., Wirz O., Wittner J., Yang J. H. M., and Yang J.

Abstract

The third edition of Flow Cytometry Guidelines provides the key aspects to consider when performing flow cytometry experiments and includes comprehensive sections describing phenotypes and functional assays of all major human and murine immune cell subsets. Notably, the Guidelines contain helpful tables highlighting phenotypes and key differences between human and murine cells. Another useful feature of this edition is the flow cytometry analysis of clinical samples with examples of flow cytometry applications in the context of autoimmune diseases, cancers as well as acute and chronic infectious diseases. Furthermore, there are sections detailing tips, tricks and pitfalls to avoid. All sections are written and peer-reviewed by leading flow cytometry experts and immunologists, making this edition an essential and state-of-the-art handbook for basic and clinical researchers.

Published
2021

8. A prospective registry to get insights into profile, management and outcome of cardiogenic shock patients

Author

Morici, N, primary, Frea, S, additional, Bertaina, M, additional, Iannacone, M, additional, Sacco, A, additional, Villanova, L, additional, Corrada, E, additional, Valente, S, additional, De Ferrari, G M, additional, Ravera, A, additional, Moltrasio, M, additional, Sionis, A, additional, Kapur, N, additional, Pappalardo, F, additional, and Tavazzi, G M, additional

Published
2022
Full Text
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9. Immunological insights in the treatment of chronic hepatitis B

Author

Iannacone, M, Andreata, F, Guidotti, L, Iannacone, Matteo, Andreata, Francesco, Guidotti, Luca G, Iannacone, M, Andreata, F, Guidotti, L, Iannacone, Matteo, Andreata, Francesco, and Guidotti, Luca G

Abstract

Hepatitis B virus (HBV) causes either acute or chronic liver diseases. Chronic hepatitis B (CHB) often progresses to the development of cirrhosis and hepatocellular carcinoma. As HBV is extremely noncytopathic, immunological events play a key role in the infection outcome. Indeed, adaptive immune responses trigger viral clearance during acute infection and viral persistence reflects the failure to generate and maintain such responses. Current therapies for patients with CHB rely on direct-acting antivirals (DAAs) that suppress viral replication without eradicating HBV from the liver. Cure of CHB may well require combining these and forthcoming DAAs with immune-stimulating approaches of different nature and function. Here, we review the relative potential of these combination therapies.

Published
2022

12. Dynamics and genomic landscape of CD8+ T cells undergoing hepatic priming

Author

Benechet, A, De Simone, G, Di Lucia, P, Cilenti, F, Barbiera, G, Le Bert, N, Fumagalli, V, Lusito, E, Moalli, F, Bianchessi, V, Andreata, F, Zordan, P, Bono, E, Giustini, L, Bonilla, W, Bleriot, C, Kunasegaran, K, Gonzalez-Aseguinolaza, G, Pinschewer, D, Kennedy, P, Naldini, L, Kuka, M, Ginhoux, F, Cantore, A, Bertoletti, A, Ostuni, R, Guidotti, L, Iannacone, M, Benechet A. P., De Simone G., Di Lucia P., Cilenti F., Barbiera G., Le Bert N., Fumagalli V., Lusito E., Moalli F., Bianchessi V., Andreata F., Zordan P., Bono E., Giustini L., Bonilla W. V., Bleriot C., Kunasegaran K., Gonzalez-Aseguinolaza G., Pinschewer D. D., Kennedy P. T. F., Naldini L., Kuka M., Ginhoux F., Cantore A., Bertoletti A., Ostuni R., Guidotti L. G., Iannacone M., Benechet, A, De Simone, G, Di Lucia, P, Cilenti, F, Barbiera, G, Le Bert, N, Fumagalli, V, Lusito, E, Moalli, F, Bianchessi, V, Andreata, F, Zordan, P, Bono, E, Giustini, L, Bonilla, W, Bleriot, C, Kunasegaran, K, Gonzalez-Aseguinolaza, G, Pinschewer, D, Kennedy, P, Naldini, L, Kuka, M, Ginhoux, F, Cantore, A, Bertoletti, A, Ostuni, R, Guidotti, L, Iannacone, M, Benechet A. P., De Simone G., Di Lucia P., Cilenti F., Barbiera G., Le Bert N., Fumagalli V., Lusito E., Moalli F., Bianchessi V., Andreata F., Zordan P., Bono E., Giustini L., Bonilla W. V., Bleriot C., Kunasegaran K., Gonzalez-Aseguinolaza G., Pinschewer D. D., Kennedy P. T. F., Naldini L., Kuka M., Ginhoux F., Cantore A., Bertoletti A., Ostuni R., Guidotti L. G., and Iannacone M.

Abstract

The responses of CD8+ T cells to hepatotropic viruses such as hepatitis B range from dysfunction to differentiation into effector cells, but the mechanisms that underlie these distinct outcomes remain poorly understood. Here we show that priming by Kupffer cells, which are not natural targets of hepatitis B, leads to differentiation of CD8+ T cells into effector cells that form dense, extravascular clusters of immotile cells scattered throughout the liver. By contrast, priming by hepatocytes, which are natural targets of hepatitis B, leads to local activation and proliferation of CD8+ T cells but not to differentiation into effector cells; these cells form loose, intravascular clusters of motile cells that coalesce around portal tracts. Transcriptomic and chromatin accessibility analyses reveal unique features of these dysfunctional CD8+ T cells, with limited overlap with those of exhausted or tolerant T cells; accordingly, CD8+ T cells primed by hepatocytes cannot be rescued by treatment with anti-PD-L1, but instead respond to IL-2. These findings suggest immunotherapeutic strategies against chronic hepatitis B infection.

Published
2019

13. Isolation of mouse Kupffer cells for phenotypic and functional studies

Author

Andreata, F, Blériot, C, Di Lucia, P, De Simone, G, Fumagalli, V, Ficht, X, Beccaria, C, Kuka, M, Ginhoux, F, Iannacone, M, Andreata, Francesco, Blériot, Camille, Di Lucia, Pietro, De Simone, Giorgia, Fumagalli, Valeria, Ficht, Xenia, Beccaria, Cristian Gabriel, Kuka, Mirela, Ginhoux, Florent, Iannacone, Matteo, Andreata, F, Blériot, C, Di Lucia, P, De Simone, G, Fumagalli, V, Ficht, X, Beccaria, C, Kuka, M, Ginhoux, F, Iannacone, M, Andreata, Francesco, Blériot, Camille, Di Lucia, Pietro, De Simone, Giorgia, Fumagalli, Valeria, Ficht, Xenia, Beccaria, Cristian Gabriel, Kuka, Mirela, Ginhoux, Florent, and Iannacone, Matteo

Abstract

Here, we provide detailed protocols for the isolation of mouse Kupffer cells – the liver-resident macrophages – for phenotypic (e.g., via flow cytometry, mass cytometry, or RNA-sequencing) analyses or for functional experiments involving cell culture. The procedures presented can be adapted for the isolation of other hepatic cell populations. For complete details on the use and execution of this protocol, please refer to De Simone et al. (2021).

Published
2021

15. Salivary gland macrophages assist tissue-resident CD8+ T cell immune surveillance

Author

Stolp, B., primary, Thelen, F., additional, Ficht, X., additional, Altenburger, L. M., additional, Ruef, N., additional, Inavalli, V. V. G. K., additional, Germann, P., additional, Page, N., additional, Moalli, F., additional, Raimondi, A., additional, Keyser, K. A., additional, Jafari, S. M. Seyed, additional, Barone, F., additional, Dettmer, M. S., additional, Merkler, D., additional, Iannacone, M., additional, Sharpe, J., additional, Schlapbach, C., additional, Fackler, O. T., additional, Nägerl, U. V., additional, and Stein, J. V., additional

Published
2019
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17. Inflammatory monocytes hinder antiviral B cell responses

Author

Sammicheli, S, Kuka, M, Di Lucia, P, de Oya, N, De Giovanni, M, Fioravanti, J, Cristofani, C, Maganuco, C, Fallet, B, Ganzer, L, Sironi, L, Mainetti, M, Ostuni, R, Larimore, K, Greenberg, P, de la Torre, J, Guidotti, L, Iannacone, M, SIRONI, LAURA, Iannacone, M., Sammicheli, S, Kuka, M, Di Lucia, P, de Oya, N, De Giovanni, M, Fioravanti, J, Cristofani, C, Maganuco, C, Fallet, B, Ganzer, L, Sironi, L, Mainetti, M, Ostuni, R, Larimore, K, Greenberg, P, de la Torre, J, Guidotti, L, Iannacone, M, SIRONI, LAURA, and Iannacone, M.

Abstract

Antibodies are critical for protection against viral infections. However, several viruses, such as lymphocytic choriomeningitis virus (LCMV), avoid the induction of early protective antibody responses by poorly understood mechanisms. We analyzed the spatiotemporal dynamics of B cell activation to show that, upon subcutaneous infection, LCMV-specific B cells readily relocate to the interfollicular and T cell areas of draining lymph nodes, where they extensively interact with CD11b+Ly6Chi inflammatory monocytes. These myeloid cells were recruited to lymph nodes draining LCMV infection sites in a type I interferon– and CCR2-dependent fashion, and they suppressed antiviral B cell responses by virtue of their ability to produce nitric oxide. Depletion of inflammatory monocytes, inhibition of their lymph node recruitment, or impairment of their nitric oxide–producing ability enhanced LCMV-specific B cell survival and led to robust neutralizing antibody production. Our results identify inflammatory monocytes as critical gatekeepers that restrain antiviral B cell responses and suggest that certain viruses take advantage of these cells to prolong their persistence within the host.

Published
2016

18. HBV Immunopathogenesis

Author

Iannacone M, Guidotti LG, Yun-Fan Liaw, Fabien Zoulim, Iannacone, M, and Guidotti, Lg

Published
2016

19. Immunosurveillance of the liver by intravascular effector CD8+ T cells

Author

Guidotti, L, Inverso, D, Sironi, L, Di Lucia, P, Fioravanti, J, Ganzer, L, Fiocchi, A, Vacca, M, Aiolfi, R, Sammicheli, S, Mainetti, M, Cataudella, T, Raimondi, A, Gonzalez Aseguinolaza, G, Protzer, U, Ruggeri, Z, Chisari, F, Isogawa, M, Sitia, G, Iannacone, M, Iannacone, M., SIRONI, LAURA, Guidotti, L, Inverso, D, Sironi, L, Di Lucia, P, Fioravanti, J, Ganzer, L, Fiocchi, A, Vacca, M, Aiolfi, R, Sammicheli, S, Mainetti, M, Cataudella, T, Raimondi, A, Gonzalez Aseguinolaza, G, Protzer, U, Ruggeri, Z, Chisari, F, Isogawa, M, Sitia, G, Iannacone, M, Iannacone, M., and SIRONI, LAURA

Abstract

Effector CD8+ T cells (CD8 TE) play a key role during hepatotropic viral infections. Here, we used advanced imaging in mouse models of hepatitis B virus (HBV) pathogenesis to understand the mechanisms whereby these cells home to the liver, recognize antigens, and deploy effector functions. We show that circulating CD8 TE arrest within liver sinusoids by docking onto platelets previously adhered to sinusoidal hyaluronan via CD44. After the initial arrest, CD8 TE actively crawl along liver sinusoids and probe sub-sinusoidal hepatocytes for the presence of antigens by extending cytoplasmic protrusions through endothelial fenestrae. Hepatocellular antigen recognition triggers effector functions in a diapedesis-independent manner and is inhibited by the processes of sinusoidal defenestration and capillarization that characterize liver fibrosis. These findings reveal the dynamic behavior whereby CD8 TE control hepatotropic pathogens and suggest how liver fibrosis might reduce CD8 TE immune surveillance toward infected or transformed hepatocytes.

Published
2015

25. Nicotine immunonanotherapeutics

Author

Iannacone M, von Andrian UH, Farokhzad OC, Alexis F, Basto P, Shi J, Moseman EA, Langer RS, Tonti E, Iannacone, M, von Andrian, Uh, Farokhzad, Oc, Alexis, F, Basto, P, Shi, J, Moseman, Ea, Langer, R, and Tonti, E

Published
2008

26. Immunonanotherapeutics that provide IgG humoral response without T-cell antigen

Author

Iannacone M, Alexis F, Basto P, Moseman EA, Shi J, Langer RS, Farokhzad OC, von Andrian U, Tonti E, Iannacone, M, Alexis, F, Basto, P, Moseman, Ea, Shi, J, Langer, R, Farokhzad, Oc, von Andrian, U, and Tonti, E

Abstract

The present invention provides compositions and systems for delivery of nanocarriers to cells of the immune system. The invention provides nanocarriers capable of stimulating an immune response in T cells and/or in B cells. The invention provides nanocarriers that comprise an immunofeature surface having a plurality of nicotine moieties. The invention provides pharmaceutical compositions comprising inventive nanocarriers. The present invention provides methods of designing, manufacturing, and using inventive nanocarriers and pharmaceutical compositions thereof. For example, the present invention nanocarriers capable of eliciting an immune response and the production of anti-nicotine antibodies.

Published
2008

27. Adjuvant incorporation in immunoanotherapeutics

Author

Alexis F, Iannacone M, Shi J, Basto P, Moseman EA, von Andrian UH, Langer RS, Farokhzad OC, Tonti E, Alexis, F, Iannacone, M, Shi, J, Basto, P, Moseman, Ea, von Andrian, Uh, Langer, R, Farokhzad, Oc, and Tonti, E

Published
2008

29. Vaccine nanotechnology

Author

von Andrian UH, Farokhzad OC, Langer RS, Junt T, Moseman EA, Zhang L, Basto P, Iannacone M, Alexis F, von Andrian, Uh, Farokhzad, Oc, Langer, R, Junt, T, Moseman, Ea, Zhang, L, Basto, P, Iannacone, M, and Alexis, F

Published
2007

30. PATOLOGIA - Fondamenti Clinicopatologici in medicina Edizione Italiana a cura di Anna Gasperi-Campani e Walter F. Grigioni

Author

GASPERI CAMPANI, ANNA, FIORENTINO, MICHELANGELO, CORTI, BARBARA, D'ERRICO, ANTONIETTA, Capelli, A., Iannacone, M., Gasperi Campani, Anna, Fiorentino, Michelangelo, Corti, Barbara, D'Errico, Antonietta, Capelli, A., and Iannacone, M.

Subjects
PATOLOGIA, MEDICINA, FONDAMENTI CLINICOPATOLOGICI
Abstract

La Patologia di Rubin, un classico della letteratura medica anglosassone, è un testo che permette agli studenti e agli studiosi di Patologia di affrontare in modo organico lo studio della materia sia nella sua parte “generale”, sia in quella “sistemica”, integrate tra di loro con grande equilibrio. Il testo presenta caratteristiche di impostazione e di rappresentazione dei concetti per molti aspetti innovative. È stata posta grande attenzione alla chiarezza espositiva e alla finalità didattica: evento del tutto eccezionale, a questo scopo il testo è stato sottoposto al vaglio di un gruppo scelto di studenti-revisori, in modo da tener conto anche della opinione dei lettori più direttamente interessati. Un gran numero di schemi e diagrammi permette di focalizzare con immediatezza e comprendere gli aspetti più complessi della materia, unitamente all’uso delle evidenziazioni e degli elenchi puntati o numerati. L’ impostazione molto moderna, con grande attenzione al livello molecolare delle informazioni più aggiornate, e l’organizzazione in sezioni distinte – epidemiologia, patogenesi, morfologia, caratteristiche cliniche – delle specifiche malattie, sono altri notevoli pregi della Patologia di Rubin.

Published
2006

32. Reduced expression of the murine p85 alpha subunit of phosphoinositide 3-kinase improves insulin signaling and ameliorates diabetes

Author

Mauvais-Jarvis F., Ueki K., Fruman D. A., Hirshman M. F., Sakamoto K., Goodyear L. J., Iannacone M., Accili D., Cantley L. C., Ronald Kahn C., Mauvais-Jarvis, F., Ueki, K., Fruman, D. A., Hirshman, M. F., Sakamoto, K., Goodyear, L. J., Iannacone, M., Accili, D., Cantley, L. C., and Ronald Kahn, C.

Abstract

A critical component of insulin action is the enzyme phosphoinositide (PI) 3-kinase. The major regulatory subunits of PI 3-kinase, p85alpha and its splice variants, are encoded by the Pik3r1 gene. Heterozygous disruption of Pik3r1 improves insulin signaling and glucose homeostasis in normal mice and mice made insulin-resistant by heterozygous deletion of the Insulin receptor and/or insulin receptor substrate-1 (IRS1) genes. Reduced expression of p85 modulates the molecular balance between this protein, the p 110 catalytic subunit of PI 3-kinase, and the IRS proteins. Thus, despite the decrease in p85alpha, PI 3-kinase activation is normal, insulin-stimulated Akt activity is increased, and glucose tolerance and insulin sensitivity are improved. Furthermore, Pik3r1 heterozygosity protects mice with genetic insulin resistance from developing diabetes. These data suggest that regulation of p85alpha levels may provide a novel therapeutic target for the treatment of type 2 diabetes. RI Iannacone, Matteo/B-3342-2008 A critical component of insulin action is the enzyme phosphoinositide (PI) 3-kinase. The major regulatory subunits of PI 3-kinase, p85α and its splice variants, are encoded by the Pik3r1 gene. Heterozygous disruption of Pik3r1 improves insulin signaling and glucose homeostasis in normal mice and mice made insulin-resistant by heterozygous deletion of the Insulin receptor and/or insulin receptor substrate-1 (IRS1) genes. Reduced expression of p85 modulates the molecular balance between this protein, the p110 catalytic subunit of PI 3-kinase, and the IRS proteins. Thus, despite the decrease in p85α, PI 3-kinase activation is normal, insulin-stimulated Akt activity is increased, and glucose tolerance and insulin sensitivity are improved. Furthermore, Pik3r1 heterozygosity protects mice with genetic insulin resistance from developing diabetes. These data suggest that regulation of p85α levels may provide a novel therapeutic target for the treatment of type 2 diabetes.

Published
2002

33. The disposal of dying cells in living tissues

Author

MANFREDI , ANGELO ANDREA M. A., Iannacone M, D'Auria F, ROVERE QUERINI , PATRIZIA, Manfredi, ANGELO ANDREA M. A., Iannacone, M, D'Auria, F, and ROVERE QUERINI, Patrizia

Published
2002

34. Anti-beta 2 glycoprotein I antibodies cause inflammation and recruit dendritic cells in platelet clearance

Author

BONDANZA , ATTILIO, MANFREDI , ANGELO ANDREA M. A., Zimmermann VS, Iannacone M, Tincani A, Balestrieri G, Sabbadini MG, ROVERE QUERINI , PATRIZIA, RI Iannacone Matteo/B 3342 2008 Tincani Angela/E 7608 2010, Bondanza, Attilio, Manfredi, ANGELO ANDREA M. A., Zimmermann, V, Iannacone, M, Tincani, A, Balestrieri, G, Sabbadini, Mg, ROVERE QUERINI, Patrizia, and RI Iannacone Matteo/B 3342 2008 Tincani Angela/E 7608, 2010

Subjects
Platelets, business.industry, Antiphospholipid antibodies, Macrophages, Antigen presentation, Inflammation, Hematology, Dendritic cell, Dendritic cells, Proinflammatory cytokine, Tumor necrosis factor-α, Immunology, medicine, Macrophage, Platelet, Platelet activation, medicine.symptom, business, Antigen-presenting cell
Abstract

SummaryScavenger phagocytes are mostly responsible for the in vivo clearance of activated or senescent platelets. In contrast to other particulate substrates, the phagocytosis of platelets does not incite pro-inflammatory responses in vivo. This study assessed the contribution of macrophages and dendritic cells (DCs) to the clearance of activated platelets. Furthermore, we verified whether antibodies against the β2 Glycoprotein I (β2GPI), which bind to activated platelets, influence the phenomenon. DCs did not per se internalise activated platelets. In contrast, macrophages efficiently phagocytosed platelets. In agreement with the uneventful nature of the clearance of platelets in vivo, phagocytosing macrophages did not release IL-1β, TNF-α or IL-10. β2GPI bound to activated platelets and was required for their recognition by anti-ββ2GPI antibodies. DCs internalised platelets opsonised by anti-ββ2GPI antibodies. The phagocytosis of opsonised platelets determined the release of TNF-α and IL-1β by DCs and macrophages. Phagocytosing macrophages, but not DCs, secreted the antiinflammatory cytokine IL-1β0. We conclude that anti-ββ2GPI antibodies cause inflammation during platelet clearance and shuttle platelet antigens to antigen presenting DCs.

Published
2001

37. A luminescent poly(amidoamine)-iridium complex as a new singlet-oxygen sensitizer for photodynamic therapy

Author

Maggioni, D, Galli, M, D'Alfonso, L, Inverso, D, Dozzi, M, Sironi, L, Iannacone, M, Collini, M, Ferruti, P, Ranucci, E, D'Alfonso, G, D'ALFONSO, LAURA, SIRONI, LAURA, COLLINI, MADDALENA, D'Alfonso, G., Maggioni, D, Galli, M, D'Alfonso, L, Inverso, D, Dozzi, M, Sironi, L, Iannacone, M, Collini, M, Ferruti, P, Ranucci, E, D'Alfonso, G, D'ALFONSO, LAURA, SIRONI, LAURA, COLLINI, MADDALENA, and D'Alfonso, G.

Abstract

A polymer complex (1P) was synthesized by binding bis(cyclometalated) Ir(ppy)2+ fragments (ppy = 2-phenylpyridyl) to phenanthroline (phen) pendants of a poly(amidoamine) copolymer (PhenISA, in which the phen pendants involved 6% of the repeating units). The corresponding molecular complex [Ir(ppy)2(bap)]+ (1M, bap = 4-(butyl-4-amino)-1,10-phenanthroline) was also prepared for comparison. In water solution 1P gives nanoaggregates with a hydrodynamic diameter of 30 nm in which the lipophilic metal centers are presumed to be segregated within polymer tasks to reduce their interaction with water. Such confinement, combined with the dilution of triplet emitters along the polymer chains, led to 1P having a photoluminescence quantum yield greater than that of 1M (0.061 vs 0.034, respectively, in an aerated water solution) with a longer lifetime of the 3MLCT excited states and a blue-shifted emission (595 nm vs 604 nm, respectively). NMR data supported segregation of the metal centers. Photoreaction of O2 with 1,5-dihydroxynaphthalene showed that 1P is able to sensitize 1O2 generation but with half the quantum yield of 1M. Cellular uptake experiments showed that both 1M and 1P are efficient cell staining agents endowed with two-photon excitation (TPE) imaging capability. TPE microscopy at 840 nm indicated that both complexes penetrate the cellular membrane of HeLa cells, localizing in the perinuclear region. Cellular photodynamic therapy tests showed that both 1M and 1P are able to induce cell apoptosis upon exposure to Xe lamp irradiation. The fraction of apoptotic cells for 1M was higher than that for 1P (74 and 38%, respectively) 6 h after being irradiated for 5 min, but cells incubated with 1P showed much lower levels of necrosis as well as lower toxicity in the absence of irradiation. More generally, the results indicate that cell damage induced by 1M was avoided by binding the iridium sensitizers to the poly(amidoamine).

Published
2015

38. In vivo flow mapping in complex vessel networks by single image correlation

Author

Sironi, L, Bouzin, M, Inverso, D, D'Alfonso, L, Pozzi, P, Cotelli, F, Guidotti, L, Iannacone, M, Collini, M, Chirico, G, SIRONI, LAURA, BOUZIN, MARGAUX, D'ALFONSO, LAURA, POZZI, PAOLO, COLLINI, MADDALENA, CHIRICO, GIUSEPPE, Sironi, L, Bouzin, M, Inverso, D, D'Alfonso, L, Pozzi, P, Cotelli, F, Guidotti, L, Iannacone, M, Collini, M, Chirico, G, SIRONI, LAURA, BOUZIN, MARGAUX, D'ALFONSO, LAURA, POZZI, PAOLO, COLLINI, MADDALENA, and CHIRICO, GIUSEPPE

Abstract

We describe a novel method (FLICS, FLow Image Correlation Spectroscopy) to extract flow speeds in complex vessel networks from a single raster-scanned optical xy-image, acquired in vivo by confocal or two-photon excitation microscopy. Fluorescent flowing objects produce diagonal lines in the raster-scanned image superimposed to static morphological details. The flow velocity is obtained by computing the Cross Correlation Function (CCF) of the intensity fluctuations detected in pairs of columns of the image. The analytical expression of the CCF has been derived by applying scanning fluorescence correlation concepts to drifting optically resolved objects and the theoretical framework has been validated in systems of increasing complexity. The power of the technique is revealed by its application to the intricate murine hepatic microcirculatory system where blood flow speed has been mapped simultaneously in several capillaries from a single xy-image and followed in time at high spatial and temporal resolution.

Published
2014

42. Sunlight Exposure and Cutaneous Human Papillomavirus Seroreactivity in Basal Cell and Squamous Cell Carcinomas of the Skin

Author

Iannacone, M. R., primary, Wang, W., additional, Stockwell, H. G., additional, O'Rourke, K., additional, Giuliano, A. R., additional, Sondak, V. K., additional, Messina, J. L., additional, Roetzheim, R. G., additional, Cherpelis, B. S., additional, Fenske, N. A., additional, Michael, K. M., additional, Waterboer, T., additional, Pawlita, M., additional, and Rollison, D. E., additional

Published
2012
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45. HPV16 genetic variation and the development of cervical cancer worldwide.

Author

Cornet, I, Gheit, T, Iannacone, M R, Vignat, J, Sylla, B S, Del Mistro, A, Franceschi, S, Tommasino, M, and Clifford, G M

Subjects
PAPILLOMAVIRUSES, CERVICAL cancer, BIOLOGICAL variation, GENETIC polymorphisms, CASE-control method, BIOBANKS, GENETICS
Abstract

Background:Factors that favour a small proportion of HPV16 infections to progress to cancer are still poorly understood, but several studies have implicated a role of HPV16 genetic variation.Methods:To evaluate the association between HPV16 genetic variants and cervical cancer risk, we designed a multicentre case-control study based on HPV16-positive cervical samples (1121 cervical cancer cases and 400 controls) from the International Agency for Research on Cancer biobank. By sequencing the E6 gene, HPV16 isolates were classified into variant lineages and the European (EUR)-lineage isolates were subclassified by the common polymorphism T350G.Results:Incidence of variant lineages differed between cases and controls in Europe/Central Asia (P=0.006, driven by an underrepresentation of African lineages in cases), and South/Central America (P=0.056, driven by an overrepresentation of Asian American/North American lineages in cases). EUR-350G isolates were significantly underrepresented in cervical cancer in East Asia (odds ratio (OR)=0.02 vs EUR-350T; 95% confidence interval (CI)=0.00-0.37) and Europe/Central Asia (OR=0.42; 95% CI=0.27-0.64), whereas the opposite was true in South/Central America (OR=4.69; 95% CI=2.07-10.66).Conclusion:We observed that the distribution of HPV16 variants worldwide, and their relative risks for cervical cancer appear to be population-dependent. [ABSTRACT FROM AUTHOR]

Published
2013
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50. Group 1 ILCs regulate T cell–mediated liver immunopathology by controlling local IL-2 availability

Author

Valeria Fumagalli, Valentina Venzin, Pietro Di Lucia, Federica Moalli, Xenia Ficht, Gioia Ambrosi, Leonardo Giustini, Francesco Andreata, Marta Grillo, Diletta Magini, Micol Ravà, Christin Friedrich, Jason D. Fontenot, Philippe Bousso, Sarah A. Gilmore, Shahzada Khan, Manuel Baca, Eric Vivier, Georg Gasteiger, Mirela Kuka, Luca G. Guidotti, Matteo Iannacone, IRCCS San Raffaele Scientific Institute [Milan, Italie], Universita Vita Salute San Raffaele = Vita-Salute San Raffaele University [Milan, Italie] (UniSR), Max Planck Research Group - The Julius-Maximiliams-Universität Würzburg, Sangamo Therapeutics brisbane, Dynamiques des Réponses immunes - Dynamics of Immune Responses, Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Gilead Sciences, Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Innate Pharma, Hôpital de la Timone [CHU - APHM] (TIMONE), ANR-17-RHUS-0007,PIONEER,Precision Immuno-Oncology for advanced Non small cell lung cancer patients with PD-1 ICI Resistance(2017), Fumagalli, V, Venzin, V, Di Lucia, P, Moalli, F, Ficht, X, Ambrosi, G, Giustini, L, Andreata, F, Grillo, M, Magini, D, Rava, M, Friedrich, C, Fontenot, J, Bousso, P, Gilmore, S, Khan, S, Baca, M, Vivier, E, Gasteiger, G, Kuka, M, Guidotti, L, Iannacone, M, Fumagalli, V., Venzin, V., Di Lucia, P., Moalli, F., Ficht, X., Ambrosi, G., Giustini, L., Andreata, F., Grillo, M., Magini, D., Rava, M., Friedrich, C., Fontenot, J. D., Bousso, P., Gilmore, S. A., Khan, S., Baca, M., Vivier, E., Gasteiger, G., Kuka, M., Guidotti, L. G., and Iannacone, M.

Subjects
Mice, Inbred BALB C, Interleukin-2 (IL-2), [SDV]Life Sciences [q-bio], Immunology, Mice, Transgenic, General Medicine, CD8-Positive T-Lymphocytes, Immunity, Innate, Hepatitis B Virus (HBV), Killer Cells, Natural, Mice, Inbred C57BL, Mice, Mice, Congenic, Group 1 innate lymphoid cells (ILCs), Animals, Interleukin-2, Lymphocytes
Abstract

Group 1 innate lymphoid cells (ILCs), which comprise both natural killer (NK) cells and ILC1s, are important innate effectors that can also positively and negatively influence adaptive immune responses. The latter function is generally ascribed to the ability of NK cells to recognize and kill activated T cells. Here, we used multiphoton intravital microscopy in mouse models of hepatitis B to study the intrahepatic behavior of group 1 ILCs and their cross-talk with hepatitis B virus (HBV)–specific CD8+T cells. We found that hepatocellular antigen recognition by effector CD8+T cells triggered a prominent increase in the number of hepatic NK cells and ILC1s. Group 1 ILCs colocalized and engaged in prolonged interactions with effector CD8+T cells undergoing hepatocellular antigen recognition; however, they did not induce T cell apoptosis. Rather, group 1 ILCs constrained CD8+T cell proliferation by controlling local interleukin-2 (IL-2) availability. Accordingly, group 1 ILC depletion, or genetic removal of their IL-2 receptor a chain, considerably increased the number of intrahepatic HBV-specific effector CD8+T cells and the attendant immunopathology. Together, these results reveal a role for group 1 ILCs in controlling T cell–mediated liver immunopathology by limiting local IL-2 concentration and have implications for the treatment of chronic HBV infection.

Published
2022
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