Browsing by Author "Burgos Cañete, Paula Isabel"

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    Humoral immune-response to a SARS-CoV-2- BNT162b2 booster in inflammatory arthritis patients who received an inactivated virus vaccine
    (BMJ PUBLISHING GROUP, 2022) Durán Santa Cruz, Josefina Gracia; Burgos Cañete, Paula Isabel; Le Corre Pérez, Monique Nicole; Ruiz-Tagle, Cinthya; Martínez Valdebenito, Constanza; Castro, Mauricio; Metcalfe Torres, Valentina Estrella; Niemann Concha, Paula Valentina; Balcells Marty, María Elvira
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    Reduced Immune Response to Inactivated Severe Acute Respiratory Syndrome Coronavirus 2 Vaccine in a Cohort of Immunocompromised Patients in Chile
    (Oxford University Press for the Infectious Diseases Society of America, 2022) Balcells Marty, María Elvira; Le Corre Pérez, Monique Nicole; Durán Santa Cruz, Josefina Gracia; Ceballos Valdivielso, María Elena Andrea; Vizcaya Altamirano, María Cecilia; Mondaca Contreras, Sebastián Patricio; Dib Marambio, Martin Javier; Rabagliati Borie, Ricardo Miguel; Sarmiento Maldonado, Mauricio; Burgos Cañete, Paula Isabel; Espinoza Sepúlveda, Manuel Antonio; Ferres Garrido, Marcela Viviana; Martínez Valdebenito, Constanza Pamela; Ruiz-Tagle Seguel, Cinthya Grace; Ortiz Koh, Catalina Alejandra; Ross Pérez, Patricio Daniel; Budnik Bitran, Sigall; Solari Gajardo, Sandra; Vizcaya Vergara, María De Los Ángeles; Lembach, Hanns; Berríos Rojas, Roslye; Melo González, Felipe; Rios Raggio, Mariana; Kalergis Parra, Alexis Mikes; Bueno Ramírez, Susan Marcela; Nervi Nattero, Bruno
    Background Inactivated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccines have been widely implemented in low- and middle-income countries. However, immunogenicity in immunocompromised patients has not been established. Herein, we aimed to evaluate immune response to CoronaVac vaccine in these patients. Methods This prospective cohort study included 193 participants with 5 different immunocompromising conditions and 67 controls, receiving 2 doses of CoronaVac 8-12 weeks before enrollment. The study was conducted between May and August 2021, at Red de Salud UC-CHRISTUS, Santiago, Chile. Neutralizing antibody (NAb) positivity, total anti-SARS-CoV-2 immunoglobulin G antibody (TAb) concentrations, and T-cell responses were determined. Results NAb positivity and median neutralizing activity were 83.1% and 51.2% for the control group versus 20.6% and 5.7% (both P < .001) in the solid organ transplant group, 41.5% and 19.2% (both P < .0001) in the autoimmune rheumatic diseases group, 43.3% (P < .001) and 21.4% (PP = .001) in the cancer with solid tumors group, 45.5% and 28.7% (both P < .001) in the human immunodeficiency virus (HIV) infection group, 64.3% and 56.6% (both differences not significant) in the hematopoietic stem cell transplant group, respectively. TAb seropositivity was also lower for the solid organ transplant (20.6%; P < .0001), rheumatic diseases (61%; P < .001), and HIV groups (70.9%; P = .003), compared with the control group (92.3%). On the other hand, the number of interferon gamma spot-forming T cells specific for SARS-CoV-2 tended to be lower in all immunocompromising conditions but did not differ significantly between groups. Conclusions Diverse immunocompromising conditions markedly reduce the humoral response to CoronaVac vaccine. These findings suggest that a boosting vaccination strategy should be considered in these vulnerable patients.
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    Therapeutic role of interferon-γ in experimental autoimmune encephalomyelitis is mediated through a tolerogenic subset of splenic CD11b+ myeloid cells
    (2024) Arellano, Gabriel; Acuña, Eric; Loda, Eileah; Moore, Lindsay; Tichauer Calderón, Juan Enrique; Castillo, Cristian; Vergara, Fabian; Burgos Cañete, Paula Isabel; Peñaloza-MacMaster, Pablo; Miller, Stephen D.; Naves, Rodrigo
    Cumulative evidence has established that Interferon (IFN)-γ has both pathogenic and protective roles in Multiple Sclerosis and the animal model, Experimental Autoimmune Encephalomyelitis (EAE). However, the underlying mechanisms to the beneficial effects of IFN-γ are not well understood. In this study, we found that IFN-γ exerts therapeutic effects on chronic, relapsing-remitting, and chronic progressive EAE models. The frequency of regulatory T (Treg) cells in spinal cords from chronic EAE mice treated with IFN-γ was significantly increased with no effect on Th1 and Th17 cells. Consistently, depletion of FOXP3-expressing cells blocked the protective effects of IFN-γ, indicating that the therapeutic effect of IFN-γ depends on the presence of Treg cells. However, IFN-γ did not trigger direct in vitro differentiation of Treg cells. In vivo administration of blocking antibodies against either interleukin (IL)-10, transforming growth factor (TGF)-β or program death (PD)-1, revealed that the protective effects of IFN-γ in EAE were also dependent on TGF-β and PD-1, but not on IL-10, suggesting that IFN-γ might have an indirect role on Treg cells acting through antigen-presenting cells. Indeed, IFN-γ treatment increased the frequency of a subset of splenic CD11b+ myeloid cells expressing TGF-β-Latency Associated Peptide (LAP) and program death ligand 1 (PD-L1) in a signal transducer and activator of transcription (STAT)-1-dependent manner. Furthermore, splenic CD11b+ cells from EAE mice preconditioned in vitro with IFN-γ and myelin oligodendrocyte glycoprotein (MOG) peptide exhibited a tolerogenic phenotype with the capability to induce conversion of naïve CD4+ T cells mediated by secretion of TGF-β. Remarkably, adoptive transfer of splenic CD11b+ cells from IFN-γ-treated EAE mice into untreated recipient mice ameliorated clinical symptoms of EAE and limited central nervous system infiltration of mononuclear cells and effector helper T cells. These results reveal a novel cellular and molecular mechanism