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    Genetic signature detected in T cell receptors from patients with severe COVID-19

    Autor: 
    Corpas, Manuel
    ;
    de Mendoza, Carmen
    ;
    Moreno-Torres, Víctor
    ;
    Pintos, Ilduara
    ;
    Seoane, Pablo
    ;
    Perkins, James R.
    ;
    Ranea, Juan A.G.
    ;
    Fatumo, Segun
    ;
    Korcsmaros, Tamas
    ;
    Martín-Villa, José Manuel
    ;
    Barreiro, Pablo
    ;
    Corral, Octavio Jorge
    Fecha: 
    2023
    Palabra clave: 
    genetics; genomics; immunology; virology; Scopus; JCR; WOS
    Revista / editorial: 
    iScience
    Citación: 
    Corpas, M., de Mendoza, C., Moreno-Torres, V., Pintos, I., Seoane, P., Perkins, J. R., ... & Soriano, V. (2023). Genetic signature detected in T cell receptors from patients with severe COVID-19. Iscience, 26(10).
    Tipo de Ítem: 
    Articulo Revista Indexada
    URI: 
    https://reunir.unir.net/handle/123456789/15442
    DOI: 
    https://doi.org/10.1016/j.isci.2023.107735
    Dirección web: 
    https://www.cell.com/iscience/fulltext/S2589-0042(23)01812-6?_returnURL=https%3A%2F%2Flinkinghub.elsevier.com%2Fretrieve%2Fpii%2FS2589004223018126%3Fshowall%3Dtrue
    Open Access
    Resumen:
    Characterization of host genetic factors contributing to COVID-19 severity promises advances on drug discovery to fight the disease. Most genetic analyses to date have identified genome-wide significant associations involving loss-of-function variants for immune response pathways. Despite accumulating evidence supporting a role for T cells in COVID-19 severity, no definitive genetic markers have been found to support an involvement of T cell responses. We analyzed 205 whole exomes from both a well-characterized cohort of hospitalized severe COVID-19 patients and controls. Significantly enriched high impact alleles were found for 25 variants within the T cell receptor beta (TRB) locus on chromosome 7. Although most of these alleles were found in heterozygosis, at least three or more in TRBV6-5, TRBV7-3, TRBV7-6, TRBV7-7, and TRBV10-1 suggested a possible TRB loss of function via compound heterozygosis. This loss-of-function in TRB genes supports suboptimal or dysfunctional T cell responses as a major contributor to severe COVID-19 pathogenesis.
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    Nombre: Genetic_signature_detected_in_T_cell_receptors.pdf
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