Person:
Sánchez Ramón, Silvia María

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First Name
Silvia María
Last Name
Sánchez Ramón
URI
https://hdl.handle.net/20.500.14352/79089
Affiliation
Universidad Complutense de Madrid
Faculty / Institute
Medicina
Department
Inmunología, Oftalmología y ORL
Area
Inmunología
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2022 - 20232
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Author: Benavente Cuesta, Celina × Subject: 612.017 ×

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    Combined Immune Defect in B-Cell Lymphoproliferative Disorders Is Associated with Severe Infection and Cancer Progression
    (Biomedicines, 2022) Ochoa Grullón, Juliana Lucía; Guevara Hoyer, Kissy; Pérez López, Cristina; Pérez de Diego, Rebeca; Peña Cortijo, Ascensión; Polo, Marta; Mateo Morales, Marta; Anguita Mandley, Eduardo; Jiménez García, Carlos; Bolaños, Estefanía; Íñigo, Belén; Medina, Fiorella; Rodríguez de la Peña, Antonia; Izquierdo Delgado, Carmen; Fuente Muñoz, Eduardo de la; Mayol, Elsa; Fernandez Arquero, Miguel; González Fernández, Ataúlfo; Benavente Cuesta, Celina; Sánchez Ramón, Silvia María
    B cell chronic lymphoproliferative diseases (B-CLPD) are associated with secondary antibody deficiency and other innate and adaptive immune defects, whose impact on infectious risk has not been systematically addressed. We performed an immunological analysis of a cohort of 83 B-CLPD patients with recurrent and/or severe infections to ascertain the clinical relevance of the immune deficiency expression. B-cell defects were present in all patients. Patients with combined immune defect had a 3.69-fold higher risk for severe infection (p = 0.001) than those with predominantly antibody defect. Interestingly, by Kaplan–Meier analysis, combined immune defect showed an earlier progression of cancer with a hazard ratio of 3.21, than predominantly antibody defect (p = 0.005). When B-CLPD were classified in low-degree, high-degree, and plasma cell dyscrasias, risk of severe disease and cancer progression significantly diverged in combined immune defect, compared with predominantly antibody defect (p = 0.001). Remarkably, an underlying primary immunodeficiency (PID) was suspected in 12 patients (14%), due to prior history of infections, autoimmune and granulomatous conditions, atypical or variegated course and compatible biological data. This first proposed SID classification might have relevant clinical implications, in terms of predicting severe infections and cancer progression, and might be applied to different B-CLPD entities.
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    Specific Cellular and Humoral Immune Responses to the Neoantigen RBD of SARS-CoV-2 in Patients with Primary and Secondary Immunodeficiency and Healthy Donors
    (Biomedicines, 2023) Mohamed, Kauzar Mohamed; Guevara Hoyer, Kissy; Jiménez García, Carlos; García Bravo, Laura; Rodríguez de la Peña, Antonia; Mediero Valeros, Beatriz; Cañizares Velázquez, Cristina; Culebras López, Esther; Cabello, Noemí; Estrada Pérez, Vicente; Fernández Arquero, Miguel; Ocaña, Alberto; Delgado-Iribarren García-Campero, Albert; Martínez-Novillo González, Mercedes; Bolaños, Estefanía; Anguita Mandly, Eduardo Luis; Peña Cortijo, Ascensión; Benavente Cuesta, Celina; Benítez Fuentes, Javier David; Pérez Segura, Pedro; Sánchez Ramón, Silvia María
    Patients with antibody deficiency disorders, such as primary immunodeficiency (PID) or secondary immunodeficiency (SID) to B-cell lymphoproliferative disorder (B-CLPD), are two groups vulnerable to developing the severe or chronic form of coronavirus disease caused by SARS-CoV-2 (COVID-19). The data on adaptive immune responses against SARS-CoV-2 are well described in healthy donors, but still limited in patients with antibody deficiency of a different cause. Herein, we analyzed spike-specific IFN-γ and anti-spike IgG antibody responses at 3 to 6 months after exposure to SARS-CoV-2 derived from vaccination and/or infection in two cohorts of immunodeficient patients (PID vs. SID) compared to healthy controls (HCs). Pre-vaccine anti-SARS-CoV-2 cellular responses before vaccine administration were measured in 10 PID patients. Baseline cellular responses were detectable in 4 out of 10 PID patients who had COVID-19 prior to vaccination, perceiving an increase in cellular responses after two-dose vaccination (p < 0.001). Adequate specific cellular responses were observed in 18 out of 20 (90%) PID patients, in 14 out of 20 (70%) SID patients and in 74 out of 81 (96%) HCs after vaccination (and natural infection in some cases). Specific IFN-γ response was significantly higher in HC with respect to PID (1908.5 mUI/mL vs. 1694.1 mUI/mL; p = 0.005). Whereas all SID and HC patients mounted a specific humoral immune response, only 80% of PID patients showed positive anti-SARS-CoV-2 IgG. The titer of anti-SARS-CoV-2 IgG was significantly lower in SID compared with HC patients (p = 0.040), without significant differences between PID and HC patients (p = 0.123) and between PID and SID patients (p =0.683). High proportions of PID and SID patients showed adequate specific cellular responses to receptor binding domain (RBD) neoantigen, with a divergence between the two arms of the adaptive immune response in PID and SID patients. We also focused on the correlation of protection of positive SARS-CoV-2 cellular response to omicron exposure: 27 out of 81 (33.3%) HCs referred COVID-19 detected by PCR or antigen test, 24 with a mild course, 1 with moderate symptoms and the remaining 2 with bilateral pneumonia that were treated in an outpatient basis. Our results might support the relevance of these immunological studies to determine the correlation of protection with severe disease and for deciding the need for additional boosters on a personalized basis. Follow-up studies are required to evaluate the duration and variability in the immune response to COVID-19 vaccination or infection.