Person:
Jiménez Reinoso, Anaïs

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First Name
Anaïs
Last Name
Jiménez Reinoso
Affiliation
Universidad Complutense de Madrid
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Now showing 1 - 9 of 9
  • Publication
    Primary T-cell immunodeficiency with functional revertant somatic mosaicism in CD247
    (Elsevier, 2017-01) Marín Marín, Ana Victoria; Jiménez Reinoso, Anaïs; Briones Contreras, Alejandro; Muñoz Ruiz, Miguel; Aydogmus, Cigdem; Pasick, Luke J; Couso, Jorge; Mazariegos, Marina S; Álvarez Prado, Ángel F; Blázquez Moreno, Alfonso; Cipe, Funda E; Haskologlu, Sule; Dogu, Figen; Morín, Matías; Moreno Pelayo, Miguel A; García Sánchez, Félix; Gil Herrera, Juana; Fernández Malavé, Edgar; Reyburn, Hugh T; Ramiro, Almudena R; Ikinciogullari,, Aydan; Recio Hoyas, María José; Regueiro González-Barros, José Ramón; Garcillán Goyoaga, Beatriz de
  • Publication
    Inherited BCL10 deficiency impairs hematopoietic and nonhematopoietic immunity
    (American Society for Clinical Investigation, 2014-11) Torres, Juan Manuel; Martínez Barricarte, Rubén; García Gómez, Sonia; Mazariegos, Marina S; Itan, Yuval; Boisson, Bertrand; Álvarez Carbajal, Rita Lucía; Jiménez Reinoso, Anaïs; del Pino, Lucía; Rodríguez Pena, Rebeca; Ferreira Martín, Antonio; Hernández Jiménez, Enrique; Toledano, Víctor; Cubillos Zapata, Carolina; Díaz Almirón, Mariana; López Collazo, Eduardo; Unzueta Roch, José L; Sánchez Ramón, Silvia María; Regueiro González-Barros, José Ramón; López Granados, Eduardo; Casanova, Jean-Laurent; Pérez de Diego, Rebeca
    Heterotrimers composed of B cell CLL/lymphoma 10 (BCL10), mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1), and caspase recruitment domain–containing (CARD) family adaptors play a role in NF-κB activation and have been shown to be involved in both the innate and the adaptive arms of immunity in murine models. Moreover, individuals with inherited defects of MALT1, CARD9, and CARD11 present with immunological and clinical phenotypes. Here, we characterized a case of autosomal-recessive, complete BCL10 deficiency in a child with a broad immunodeficiency, including defects of both hematopoietic and nonhematopoietic immunity. The patient died at 3 years of age and was homozygous for a loss-of-expression, loss-of function BCL10 mutation. The effect of BCL10 deficiency was dependent on the signaling pathway, and, for some pathways, the cell type affected. Despite the noted similarities to BCL10 deficiency in mice, including a deficient adaptive immune response, human BCL10 deficiency in this patient resulted in a number of specific features within cell populations. Treatment of the patient’s myeloid cells with a variety of pathogen-associated molecular pattern molecules (PAMPs) elicited a normal response; however, NF-κB–mediated fibroblast functions were dramatically impaired. The results of this study indicate that inherited BCL10 deficiency should be considered in patients with combined immunodeficiency with B cell, T cell, and fibroblast defects.
  • Publication
    Lymphocyte integration of complement cues
    (Elsevier, 2018-03-08) Marín Marín, Ana Victoria; Cárdenas, Paula P; Jiménez Reinoso, Anaïs; Muñoz Ruiz, Miguel; Regueiro González-Barros, José Ramón
    We address current data, views and puzzles on the emerging topic of regulation of lymphocytes by complement proteins or fragments. Such regulation is believed to take place through complement receptors (CR) and membrane complement regulators (CReg) involved in cell function or protection, respectively, including intracellular signalling. Original observations in B cells clearly support that complement cues through CR improve their performance. Other lymphocytes likely integrate complement-derived signals, as most lymphoid cells constitutively express or regulate CR and CReg upon activation. CR-induced signals, particularly by anaphylatoxins, clearly regulate lymphoid cell function. In contrast, data obtained by CReg crosslinking using antibodies are not always confirmed in human congenital deficiencies or knock-out mice, casting doubts on their physiological relevance. Unsurprisingly, human and mouse complement systems are not completely homologous, adding further complexity to our still fragmentary understanding of complement-lymphocyte interactions.
  • Publication
    Human plasma C3 is essential for the development of memory B, but not T, lymphocytes
    (Elsevier, 2018-03) Jiménez Reinoso, Anaïs; Marín Marín, Ana Victoria; Subias, Marta; López Lera, Alberto; Román Ortiz, Elena; Payne, Kathryn; Ma, Cindy S; Arbore, Giuseppina; Kolev, Martín; Freeley, Simón J; Kemper, Claudia; Tangye, Stuart G; Fernández Malavé, Edgar; Rodríguez de Córdoba, Santiago; López Trascasa, Margarita; Regueiro González-Barros, José Ramón
  • Publication
    Impacto de la deficiencia de C3 plasmático en la diferenciación y función leucocitaria
    (Universidad Complutense de Madrid, 2017-12-20) Jiménez Reinoso, Anaïs; Regueiro González-Barros, José R.
    El papel del complemento en la inmunobiología ha evolucionado notablemente desde que fue descrito inicialmente como un elemento clave de la inmunidad innata. Lejos de su visión tradicional como un simple elemento termolábil que complementaba la eliminación de microbios mediada por anticuerpos, hoy día el sistema de complemento es considerado como un puente entre la inmunidad innata y adaptativa1. De las más de 50 proteínas que lo componen, la proteína C3 es el eje central en el que convergen sus tres vías de activación y por ello, tiene un fuerte impacto en la regulación de la biología leucocitaria, especialmente en linfocitos T, B y células dendríticas (DC). Los antígenos solubles opsonizados por fragmentos plasmáticos de C3d(g) se unen a través de su receptor CD21 e inducen el reclutamiento de CD19 y CD81 para formar el co-receptor de linfocitos B, reduciendo significativamente el umbral de activación del receptor de linfocitos B2. El receptor CD21, también conocido como receptor de complemento 2, es expresado por células dendríticas foliculares que capturan antígenos opsonizados con C3d(g) en los centros germinales de los órganos linfoides secundarios, favoreciendo la maduración de la afinidad, el cambio de isotipo y la adquisición de memoria de linfocitos B naíf o primados3. A pesar de que hace años ya se apuntó a una síntesis extra-hepática del complemento, con el tiempo han ido creciendo las evidencias que respaldan su síntesis local por diferentes tipos leucocitarios4. De hecho, los recientes hallazgos que exponen la existencia de un sistema de activación de C3 intracelular diferente al conocido plasmático con importantes consecuencias para la homeostasis y función de los linfocitos T ponen de manifiesto el alcance de la influencia de C3 en mamíferos5. En este contexto se ha visto que tanto los linfocitos T como las DC sintetizan fragmentos de C3 que actúan de forma autocrina y paracrina, favoreciendo la función de presentación antigénica de las DC e induciendo funciones efectoras en los linfocitos T6...
  • Publication
    Human congenital T-cell receptor disorders
    (Canadian Science Publishing, 2015) Marín Marín, Ana Victoria; Garcillán Goyoaga, Beatriz de; Jiménez Reinoso, Anaïs; Muñoz Ruiz, Miguel; Briones Contreras, Alejandro; Fernández Malavé, Edgar; Recio Hoyas, María José; Regueiro González-Barros, José Ramón
    Immunodeficiencies of most T-cell receptor (TCR) components (TCRID) have been reported in almost 40 patients worldwide who have also, at times, shown signs of autoimmunity. We updated their clinical, immunological, and molecular features with an emphasis on practical diagnosis, as the range of the disorder grows in complexity with new partial defects. Cellular and animal models are also reviewed and in some cases reveal their limitations for predicting TCRID immunopathology.
  • Publication
    gd T lymphocytes in the diagnosis of human T cell receptor immunodeficiencies
    (Frontiers Media, 2015-06-25) Garcillán Goyoaga, Beatriz de; Marín Marín, Ana Victoria; Jiménez Reinoso, Anaïs; Briones Contreras, Alejandro; Muñoz Ruiz, Miguel; García León, María J; Gil Calle, Juana Nelly; Allende Martínez, Luis Miguel; Martínez Naves, Eduardo; Toribio, Maria Luisa; Regueiro González-Barros, José Ramón
    Human T cell receptor (TCR) immunodeficiencies (TCRID) are rare autosomal recessive disorders caused by mutations affecting TCR, CD3, or CD247 chains, which share developmental, functional, and TCR expression defects (1). Their rapid diagnosis is fundamental for patient survival and early hematopoietic stemcell transplantation.Here,we propose that studying gd T cells, which are often neglected, can be helpful for a timely diagnosis. We thus offer a diagnostic flowchart and some lab tricks based on published cases.
  • Publication
    Complement in basic processes of the cell
    (Elsevier, 2016-12-03) Jiménez Reinoso, Anaïs; Marín Marín, Ana Victoria; Regueiro González-Barros, José Ramón
    The complement system is reemerging in the last few years not only as key element of innate immunityagainst pathogens, but also as a main regulator of local adaptive responses, affecting dendritic cells as wellas T and B lymphocytes. We review data showing that leucocytes are capable of significant autocrine syn-thesis of complement proteins, and express a large range of complement receptors, which in turn regulatetheir differentiation and effector functions while cross talking with other innate receptors such as Toll-like receptors. Other unconventional roles of complement proteins are reviewed, including their impactin non-leukocytes and their intracellular cleavage by vesicular proteases, which generate critical cuesrequired for T cell function. Thus, leucocytes are very much aware of complement-derived information,both extracellular and intracellular, to elaborate their responses, offering rich avenues for therapeuticintervention and new hypothesis for conserved major histocompatibility complex complotypes.
  • Publication
    CD3G or CD3D Knockdown in Mature, but Not Immature, T Lymphocytes Similarly Cripples the Human TCRαβ Complex
    (Frontiers Media, 2021-06-25) Garcillán Goyoaga, Beatriz de; Fuentes, Patricia; Marín Marín, Ana Victoria; Fernández Megido, Rebeca; Chacón Arguedas, Carlos Daniel; S. Mazariegos, Marina; González Laborda, Raquel; Jiménez Reinoso, Anaïs; Muñoz Ruiz, Miguel; Cárdenas Mastracusa, Paula; Fernández-Malavé, Edgar; Toribio, Maria Luisa; Regueiro González-Barros, José Ramón
    The human αβ T-cell receptor (TCR) is composed of a variable heterodimer (TCRαβ) and three invariant dimers (CD3γε, CD3δε, and ζζ/CD2472). The role of each invariant chain in the stepwise interactions among TCR chains along the assembly is still not fully understood. Despite the high sequence homology between CD3γ and CD3δ, the clinical consequences of the corresponding immunodeficiencies (ID) in humans are very different (mild and severe, respectively), and mouse models do not recapitulate findings in human ID. To try to understand such disparities, we stably knocked down (KD) CD3D or CD3G expression in the human Jurkat T-cell line and analyzed comparatively their impact on TCRαβ assembly, transport, and surface expression. The results indicated that TCR ensembles were less stable and CD3ε levels were lower when CD3γ, rather than CD3δ, was scarce. However, both defective TCR ensembles were strongly retained in the ER, lacked ζζ/CD2472, and barely reached the T-cell surface (<11% of normal controls) in any of the CD3 KD cells. This is in sharp contrast to human CD3γ ID, whose mature T cells express higher levels of surface TCR (>30% vs. normal controls). CD3 KD of human T-cell progenitors followed by mouse fetal thymus organ cultures showed high plasticity in emerging immature polyclonal T lymphocytes that allowed for the expression of significant TCR levels which may then signal for survival in CD3γ, but not in CD3δ deficiency, and explain the immunological and clinical disparities of such ID cases.