Citations 2
Immune checkpoint dysregulation in COVID-19 pathogenesis and disease severity.
Villalba, Julian A. , Shih, Angela , Alba, George A. , Loyola-Rodríguez, Georgina, Alcántara, Ismael Ramírez, Ferreira, Luíz Carlos de Lima , Stigliano, Egidio, Hirschbühl, Klaus , Argueta, Allan , Ackermann, Maximillian , Werlein, Christopher , Uribe‐Uribe, Norma , Vázquez-Benítez, Greissy, Tzankov, Alexandar , Stalder, Anna K. , Francesqui, Joel , Osborn, Michael , Hanley, Brian , Johnston, Robert, Lacy, J. Matthew , Marshall, Desiree A. , Schwensen, Hanna Ferløv , Okudela, Koji , Flikweert, Antine, Iles, Linda , d’Amati, Giulia , Träger, Lene Hoffmann , Çınar, Hüseyin, Aguiar, Diego , Dolhnokoff, Marisa, Chilosi, Marco , Salmon, I, Colville‐Ebeling, Bonnie, Poissy, Julien , Haahr, Martha Kirstine , Reyes, Fabiola, Parry, Blair A. , Garlin, Michelle, Hilburn, Caroline F., ELLIOTT, G. A., Rosas, Iván O. , Sade-Feldman, Moshe , Hacohen, Nir , Baden, Lindsey R. , Li, Jonathan Z. , Schaller, Tina , Gigli, L, Macciò, Umberto , Yick, David C.Y., Bruni, Barbara, Pernazza, Angelina , Mauad, Thaís , Dubini, Alessandra, Hartmann, Arndt, Remmelink, Myriam , Aviles, Alexis J., Barth, Jamie L., Boyraz, Bariş , Araujo-Medina, Milagros, Mendez-Pena, Javier E., Chebib, Ivan , Hung, Yin P. , Rosales, Ivy A. , Smith, Rex-Neal, Hung, Yin P , Tzankov, Alexandar , Li, Yijia , Poli, Sergio , Kunitoki, Keiko , Mehta, Arnav , Santana, Monique Freire , Lacerda, Marcus , Dell’Aquila, Marco , Arena, Vincenzo , Calabrese, Fiorella , Pezzuto, Federica , Märkl, Bruno , Lozano, Maria, Jonigk, Danny David , Pomara, Cristoforo , Salerno, Monica , Salas, Clara , Martínez, Daniel, Parra-Medina, Rafael Santiago , Bradley, Benjamin T. , Chen, Sonja , Varga, Zsuzsanna , Steinestel, Konrad , Harper, Holly , Aiolfi, Alberto , Scendoni, Roberto , Fabro, Alexandre Todorovic , Doglioni, Claudio , Rossi, Giulio , Poletti, Venerino , Herrmann, Martin , Pugh, Matthew , Yan, Lei , Gentili, Matteo , Garlin, Michelle A., Lo, Ying‐Chun , Elliott, Grant, Martínez, Leonardo , Stone, James R. , Colvin, Robert B. , Goldberg, Marcia B. , Filbin, Michael R. , Mino-Kenudson, Mari A. , Kröncke, Thomas J. , Gigli, Laura Álvarez, Sessa, Francesco , Caltabiano, Rosario , Menter, Thomas , Sellarés, Jacobo , Storgaard, Merete , Hamilton‐Dutoit, Stephen , Dannheim, Katelyn , Witte, Hanno Maximilian , Bona, Davide , Leth, Peter Mygind , Banner, Jytte , Batah, Sabrina Setembre , Silva, Luiz Fernando Ferraz da , Duarte‐Neto, Amaro Nunes , Saldiva, Paulo Hilário Nascimento , Munoz, Luis Enrique , Jensen, T. , Brøchner, Christian Beltoft , Gibier, Jean‐Baptiste , Gilbert, Andrea , Madrigal, Emilio , Ly, Amy , Hariri, Lida P. , Caldwell, Nicholas J
No container title available | October 2, 2024 | Volume: No volume available | Issue: No issue available | Pages: No page available
Abstract Accumulating evidence suggests dysregulated immune checkpoint (IC) signaling can exacerbate COVID-19 severity, but the role of these molecules in the pathogenesis of fatal COVID-19-related diffuse alveolar damage (DAD) remains elusive. Understanding how IC proteins influence acute lung injury due to COVID-19 can provide insights into potential therapeutic strategies to modulate immune responses and improve patient outcomes. Here, in a single-center autopsy cohort, we determined the cellular localization of ICs in lung tissue from cases of fatal COVID-19, DAD-comparators, and non-fibrotic controls by using immunohistochemistry, and investigated their association with clinical outcomes. We expanded our findings by performing analyses of publicly available single-cell RNA sequencing datasets from patients with fatal COVID-19 and non-fibrotic controls. We demonstrated the presence of protein-protein interaction networks of ICs in the lung cellular niche by performing transcriptomic profiling of lung tissue-derived RNA counts from patients with fatal COVID-19. Further, we leveraged data from the largest international, multi-center COVID-19 autopsy cohort and validated that, among patients with fatal COVID-19, those with higher PD-L1/CD274 expression in lung endothelial cells had more rapid clinical deterioration. Lastly, in a cohort of individuals with early COVID-19, IC plasma protein levels were elevated in those with persistent SARS-CoV-2 RNAemia and adverse clinical outcomes. Collectively, our data provide unique pathological insights into the role of IC dysregulation and differential disease severity in COVID-19.
Balloon cell nevus in children: Report of three cases of the scalp and review
Micali, Giuseppe , Verzì, Anna Elisa , Puglisi, Davide Francesco, Quattrocchi, Enrica , Lacarrubba, Francesco , Lacarrubba, Francesco , Caltabiano, Rosario
Pediatric Dermatology | September 28, 2020 | Volume: 38 | Issue: 1 | Pages: 198-201
AbstractBalloon cell nevus (BCN) is a histopathological variant of cutaneous acquired melanocytic nevi characterized by junctional and/or dermal nests of large cells with a clear and foamy cytoplasm which has rarely been described in children. Three cases of BCN firstly reported on the scalp in two pediatric patients are presented along with a literature review. Dermoscopy is particularly indicated in those pigmented lesions showing a yellowish hue, in ruling out in real time those disorders that may clinically be similar such as xanthogranuloma and sebaceous nevus, and to suggest the diagnosis of BCN. The final diagnosis, however, is established by histopathological examination.