dc.contributor | Vall d'Hebron Barcelona Hospital Campus |
dc.contributor.author | Julia Cano, Antonio |
dc.contributor.author | Bonafonte Pardàs, Irene |
dc.contributor.author | Gomez Moruno, Antonio |
dc.contributor.author | Lopez Lasanta, Maria America |
dc.contributor.author | Lopez Corbeto, Mireia |
dc.contributor.author | Martinez Mateu, Sergio Hilario |
dc.contributor.author | Llados Segura, Jordi Francesc |
dc.contributor.author | Marsal Barril, Sara |
dc.date.accessioned | 2022-01-14T11:16:03Z |
dc.date.available | 2022-01-14T11:16:03Z |
dc.date.issued | 2021-06-01 |
dc.identifier.citation | Julià A, Bonafonte-Pardàs I, Gómez A, López-Lasanta M, López-Corbeto M, Martínez-Mateu SH, et al. Targeting of the CD80/86 proinflammatory axis as a therapeutic strategy to prevent severe COVID-19. Sci Rep. 2021 Jun 1;11:11462. |
dc.identifier.issn | 2045-2322 |
dc.identifier.uri | https://hdl.handle.net/11351/6803 |
dc.description | Coronavirus SARS-CoV-2; COVID-19; 2019-nCoV; Inflammatory diseases; Target identification; Viral infection |
dc.description.abstract | An excessive immune response known as cytokine storm is the hallmark of severe COVID-19. The cause of this cytokine rampage is yet not known. Based on recent epidemiological evidence, we hypothesized that CD80/86 signaling is essential for this hyperinflammation, and that blocking this proinflammatory axis could be an effective therapeutic approach to protect against severe COVID-19. Here we provide exploratory evidence that abatacept, a drug that blocks CD80/86 co-stimulation, produces changes at the systemic level that are highly antagonistic of the proinflammatory processes elicited by COVID-19. Using RNA-seq from blood samples from a longitudinal cohort of n = 38 rheumatic patients treated with abatacept, we determined the immunological processes that are significantly regulated by this treatment. We then analyzed available blood RNA-seq from two COVID19 patient cohorts, a very early cohort from the epicenter of the pandemic in China (n = 3 COVID-19 cases and n = 3 controls), and a recent and larger cohort from the USA (n = 49 severe and n = 51 mild COVD-19 patients). We found a highly significant antagonism between SARS-CoV-2 infection and COVID-19 severity with the systemic response to abatacept. Analysis of previous single-cell RNA-seq data from bronchoalveolar lavage fluid from mild and severe COVID-19 patients and controls, reinforce the implication of the CD80/86 proinflammatory axis. Our functional results further support abatacept as a candidate therapeutic approach to prevent severe COVID-19. |
dc.language.iso | eng |
dc.publisher | Nature Research |
dc.relation.ispartofseries | Scientific Reports;11 |
dc.rights | Attribution 4.0 International |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/ |
dc.source | Scientia |
dc.subject | COVID-19 (Malaltia) - Tractament |
dc.subject | Medicaments immunosupressors - Ús terapèutic |
dc.subject | Artritis reumatoide - Tractament |
dc.subject.mesh | Coronavirus Infections |
dc.subject.mesh | Immunosuppressive Agents |
dc.subject.mesh | Arthritis, Rheumatoid |
dc.subject.mesh | /drug therapy |
dc.title | Targeting of the CD80/86 proinflammatory axis as a therapeutic strategy to prevent severe COVID-19 |
dc.type | info:eu-repo/semantics/article |
dc.identifier.doi | 10.1038/s41598-021-90797-0 |
dc.subject.decs | infecciones por Coronavirus |
dc.subject.decs | inmunosupresores |
dc.subject.decs | artritis reumatoide |
dc.subject.decs | /farmacoterapia |
dc.type.version | info:eu-repo/semantics/publishedVersion |
dc.audience | Professionals |
dc.contributor.organismes | Institut Català de la Salut |
dc.contributor.authoraffiliation | [Julià A, Bonafonte-Pardàs I, Gómez A, López-Lasanta M, López-Corbeto M, Martínez-Mateu SH, Lladós J, Marsal S] Grup de Recerca en Reumatologia, Servei de Reumatologia, Vall d’Hebron Hospital Institut de Recerca (VHIR), Barcelona, Spain |
dc.identifier.pmid | 34075090 |
dc.identifier.wos | 000660845500005 |
dc.relation.projectid | info:eu-repo/grantAgreement/EC/H2020/848028 |
dc.rights.accessrights | info:eu-repo/semantics/openAccess |