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Raquel Planas

Researcher at University of Zurich

Publications -  34
Citations -  1613

Raquel Planas is an academic researcher from University of Zurich. The author has contributed to research in topics: Immune system & Antigen. The author has an hindex of 23, co-authored 33 publications receiving 1357 citations. Previous affiliations of Raquel Planas include Autonomous University of Barcelona & University of Hamburg.

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Peripheral and Islet Interleukin-17 Pathway Activation Characterizes Human Autoimmune Diabetes and Promotes Cytokine-Mediated β-Cell Death

TL;DR: It is shown that IL-17 mediates significant and reproducible enhancement of IL-1β/interferon (IFN)-γ–induced and tumor necrosis factor (TNF)-α/IFN-γ-induced apoptosis in human islets, rat β-cells, and INS-1E cells, in association with significant upregulation of β-cell IL17RA expression via activation of the transcription factors STAT1 and nuclear factor (NF)-κB.
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Natalizumab treatment perturbs memory- and marginal zone-like B-cell homing in secondary lymphoid organs in multiple sclerosis.

TL;DR: The ability of natalizumab to influence B‐cell migration and homeostasis through the splenic MZ, where JCV has been detected, adds to the list of nalozumab effects and may contribute to PML development by disseminating JCV.
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Gene expression profiles for the human pancreas and purified islets in Type 1 diabetes: new findings at clinical onset and in long-standing diabetes

TL;DR: In this paper, the authors reported whole genome transcript analysis validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and correlated with immunohistological observations for four Type 1 diabetes patients and for purified islets from two of them.
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GDP-l-fucose synthase is a CD4+ T cell–specific autoantigen in DRB3*02:02 patients with multiple sclerosis

TL;DR: GDP-l-fucose synthase is an autoantigen recognized by cerebrospinal fluid–infiltrating CD4+ T cells from HLA-DRB3*–positive patients with multiple sclerosis, and the possible role of this antigen as an inducer or driver of pathogenic autoimmune responses in multiple sclerosis is suggested.