Virtualización y ampliación del material docente para las prácticas de laboratorio de la asignatura de Biología Celular e Histología

Este proyecto pretende facilitar el aprendizaje y mejorar los conocimientos de los alumnos del Grado en Biología sobre los temas tratados en las prácticas de Biología Celular, mediante la elaboración de diverso material docente adicional

Altered thymocyte development observed in EphA4-deficient mice courses with changes in both thymic epithelial and extracellular matrix organization

Eph receptors and their ligands, Ephrins, are involved in the thymocyte-thymic epithelial cell (TEC) interactions, key for the functional maturation of both thymocytes and thymic epithelium. Several years ago, we reported that the lack of EphA4, a Eph of the subfamily A, coursed with reduced proportions of double positive (DP) thymocytes apparently due to an altered thymic epithelial stroma [Munoz et al. in J Immunol 177:804–813, 2006]. In the present study, we reevaluate the lymphoid, epithelial, and extracellular matrix (ECM) phenotype of EphA4−/− mice grouped into three categories with respect to their proportions of DP thymocytes. Our results demonstrate a profound hypocellularity, specifc alterations of T cell diferentiation that afected not only DP thymocytes, but also double negative and single positive T cell subsets, as well as the proportions of positively and negatively selected thymocytes. In correlation, thymic histological organization changed markedly, especially in the cortex, as well as the proportions of both Ly51+UEA-1− cortical TECs and Ly51−UEA-1+ medullary TECs. The alterations observed in the expression of ECM components (Fibronectin, Laminin, Collagen IV), integrin receptors (VLA-4, VLA-6), chemokines (CXCL12, CCL25, CCL21) and their receptors (CXCR4, CCR7, CCR9) and in vitro transwell assays on the capacity of migration of WT and mutant thymocytes suggest that the lack of EphA4 alters T-cell diferentiation by presumably afecting cell adhesion between TECs and T-TEC interactions rather than by thymocyte migration

Digitalización de la histoteca de las prácticas de Organografía Microscópica

Histoteca digital para que los alumnos puedan consultar un material gráfico actualizado y concreto, similar a lo que observan en el microscopio cuando realizan sus prácticas de Organografía de la asignatura de “Organografía microscópica” del Grado en Biología

ICAP-1 loss impairs CD8+ thymocyte development and leads to reduced marginal zone B cells in mice

ICAP-1 regulates β1-integrin activation and cell adhesion. Here, we used ICAP-1-null mice to study ICAP-1 potential involvement during immune cell development and function. Integrin α4β1-dependent adhesion was comparable between ICAP-1-null and control thymocytes, but lack of ICAP-1 caused a defective single-positive (SP) CD8+ cell generation, thus, unveiling an ICAP-1 involvement in SP thymocyte development. ICAP-1 bears a nuclear localization signal and we found it displayed a strong nuclear distribution in thymocytes. Interestingly, there was a direct correlation between the lack of ICAP-1 and reduced levels in SP CD8+ thymocytes of Runx3, a transcription factor required for CD8+ thymocyte generation. In the spleen, ICAP-1 was found evenly distributed between cytoplasm and nuclear fractions, and ICAP-1–/– spleen T and B cells displayed upregulation of α4β1-mediated adhesion, indicating that ICAP-1 negatively controls their attachment. Furthermore, CD3+- and CD19+-selected spleen cells from ICAP-1-null mice showed reduced proliferation in response to T- and B-cell stimuli, respectively. Finally, loss of ICAP-1 caused a remarkable decrease in marginal zone B- cell frequencies and a moderate increase in follicular B cells. Together, these data unravel an ICAP-1 involvement in the generation of SP CD8+ thymocytes and in the control of marginal zone B-cell numbers

Metodología para la auditoría de sistemas Big Data.

El Big Data ha supuesto una tecnología disruptiva que ha cambiado la forma en la que se hacen los negocios. Ahora, las organizaciones disponen de sistemas que son capaces de tomar decisiones en base a análisis ejecutados sobre los datos recogidos de sus actividades u otras fuentes. Big Data se encarga de almacenar, manipular y analizar estos datos. Esto puede suponer un problema si estos datos no están siendo gestionados de forma correcta. El entorno Big Data dentro de una organización debe estar sujeto a unas normas que aseguren la correcta manipulación de este, que puede abarcar desde las técnicas de tratamiento de los datos dentro del sistema hasta el cumplimiento de la regulación presente en el país en el que opera la organización. Por ello, estos sistemas necesitan ser revisados y aprobados dentro de un marco de auditoría que recoja las características propias de un sistema Big Data. Este TFM propone una metodología de auditoría para esta clase de sistemas como objetivo principal. Con esta metodología el auditor será capaz de identificar, probar y verificar los controles específicos implementados en las distintas partes de un sistema Big Data.Big Data is a groundbreaker technology that has changed the way business is done. Nowadays, organizations have systems which can make decisions based on analysis of data they collect either from their own activities or from other sources. Big Data is in charge of storing, handling and analyzing that data. This could pose a problem if data is not managed correctly. Within any organization, Big Data must be subject to regulations which assure its correct use. These regulations may include data processing techniques of the system, as well as the compliance with the current regulation of the country where the organization operates. Therefore, these systems need to be revised and approved within an audit framework which holds the specific characteristics of a Big Data system. This essay puts forward an auditing methodology for this type of systems, as its main objective. With this methodology , the auditor will be able to identify, test and verify the specific controls implemented in the different parts of a Big Dat

Organización de la red epitelial tímica en ratones deficientes en los receptores Eph B2 y-o Eph B3

Tesis inédita de la Universidad Complutense de Madrid, Facultad de Ciencias Biológicas, Departamento de Biología Celular, leída el 18-05-2007Depto. de Biología CelularFac. de Ciencias BiológicasTRUEProQuestpu

Altered Maturation of Medullary TEC in EphB-Deficient Thymi Is Recovered by RANK Signaling Stimulation

In the present study, the relevance of EphB2 and EphB3 tyrosine kinase receptors for the maturation of medullary thymic epithelial cells (TECs) is analyzed. The absence of both molecules, but particularly that of EphB2, courses with altered maturation of medullary Cld3,4hiSSEA1+ epithelial progenitor cells, mature medulla epithelial cells, defined by the expression of specific cell markers, including UEA1, MHCII, CD40, CD80, and AIRE, and reduced expansion of medullary islets. In vivo assays demonstrate that these changes are a consequence of the absence of EphBs in both TECs and thymocytes. On the other hand, the changes, that remains in the adult thymus, correlated well with reduced proportions of E15.5 Vγ5+RANKL+ cells in EphB-deficient thymi that could result in decreased stimulation of RANK+ medullary TECs to mature, a fact that was confirmed by recovering of proportions of both CD40hiCD80+ and MHCIIhiUEA1+ mature medullary TECs of mutant E14.5 alymphoid thymic lobes by agonist anti-RANK antibody treatment. Accordingly, the effects of EphB deficiency on medullary TECs maturation are recovered by RANK stimulation

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Image_2_Altered Maturation of Medullary TEC in EphB-Deficient Thymi Is Recovered by RANK Signaling Stimulation.PDF

<p>In the present study, the relevance of EphB2 and EphB3 tyrosine kinase receptors for the maturation of medullary thymic epithelial cells (TECs) is analyzed. The absence of both molecules, but particularly that of EphB2, courses with altered maturation of medullary Cld3,4^hiSSEA1⁺ epithelial progenitor cells, mature medulla epithelial cells, defined by the expression of specific cell markers, including UEA1, MHCII, CD40, CD80, and AIRE, and reduced expansion of medullary islets. In vivo assays demonstrate that these changes are a consequence of the absence of EphBs in both TECs and thymocytes. On the other hand, the changes, that remains in the adult thymus, correlated well with reduced proportions of E15.5 Vγ5⁺RANKL⁺ cells in EphB-deficient thymi that could result in decreased stimulation of RANK⁺ medullary TECs to mature, a fact that was confirmed by recovering of proportions of both CD40^hiCD80⁺ and MHCII^hiUEA1⁺ mature medullary TECs of mutant E14.5 alymphoid thymic lobes by agonist anti-RANK antibody treatment. Accordingly, the effects of EphB deficiency on medullary TECs maturation are recovered by RANK stimulation.</p

Peripheral T‑cell responses of EphB2‑ and EphB3‑deficient mice in a model of collagen‑induced arthritis

2024 Acuerdos transformativos CRUE-CSICBoth EphB2- and EphB3-deficient mice exhibit profound histological alterations in the thymic epithelial network but few changes in T-cell differentiation, suggesting that this organization would be sufficient to produce functional T lymphocytes. Also, other antigen-presenting cells involved in immunological education could substitute the thymic epithelium. Accordingly, we found an increased frequency of plasmacytoid dendritic cells but not of conventional dendritic cells, medullary fibroblasts or intrathymic B lymphocytes. In addition, there are no lymphoid infiltrates in the organs of mutant mice nor do they contain circulating autoantibodies. Furthermore, attempts to induce arthritic lesions after chicken type II collagen administration fail totally in EphB2-deficient mice whereas all WT and half of the immunized EphB3−/− mice develop a typical collagen-induced arthritis. Our results point out that Th17 cells, IL4-producing Th2 cells and regulatory T cells are key for the induction of disease, but mutant mice appear to have deficits in T cell activation or cell migration properties. EphB2−/− T cells show reduced in vitro proliferative responses to anti-CD3/anti-CD28 antibodies, produce low levels of anti-type II collagen antibodies, and exhibit low proportions of T follicular helper cells. On the contrary, EphB3−/− lymph node cells respond accurately to the different immune stimuli although in lower levels than WT cells but show a significantly reduced migration in in vitro transwell assays, suggesting that no sufficient type II collagen-dependent activated lymphoid cells reached the joints, resulting in reduced arthritic lesions.Unión Europea. NextGenerationEU. Plan de Recuperación Transformación y ResilienciaMinisterio de Ciencia, Innovación y UniversidadesInstituto de Salud Carlos IIIDepto. de Biología CelularFac. de Ciencias BiológicasTRUEpu