Publications by authors named "Jose Luis Sanchez-Trincado"

Background: Polymerized allergoids conjugated with mannan represent a novel approach of allergen immunotherapy targeting dendritic cells. In this study, we aimed to determine the optimal dose of mannan-allergoid conjugates derived from grass pollen ( and ) administered via either the subcutaneous or sublingual route.

Methods: A randomized, double-blind, placebo-controlled trial with a double-dummy design was conducted, involving 162 participants across 12 centers in Spain.

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Article Synopsis
  • Correction of mis-splicing events is being explored as a therapeutic strategy for neurological diseases like spinal muscular atrophy and Huntington's disease, which arise from splicing-related mutations.
  • Next-generation RNA sequencing has enabled the detailed study of mis-spliced genes in diseases, although challenges exist in analyzing brain tissue due to cell loss and inflammation in neurodegenerative conditions.
  • The study utilized intersect-RNA-seq to identify common mis-splicing patterns in Huntington's disease, leading to potential new therapeutic targets related to the disease's progression.
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The phagocytic integrins and complement receptors αβ/CR3 and αβ/CR4 are classically associated with the phagocytosis of iC3b-opsonized particles. The activation of this receptor is dependent on signals derived from other receptors (inside-out signaling) with the crucial involvement of the Rap1-RIAM-Talin-1 pathway. Here, we analyze the implication of RIAM and its binding partner VASP in the signaling events occurring downstream of β integrins (outside-in) during complement-mediated phagocytosis.

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Type 1 diabetes (T1D) results from the destruction of pancreatic β-cells by the immune system, and CD8 T lymphocytes are critical actors in this autoimmune response. Pancreatic islets are surrounded by a mesh of nervous cells, the peri-insular Schwann cells, which are also targeted by autoreactive T lymphocytes and express specific antigens, such as the neurotrophic factor S100-β. Previous work has shown increased proliferative responses to whole S100-β in both human T1D patients and the nonobese diabetic (NOD) mouse model.

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