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Abel Suárez-Fueyo

Researcher at Beth Israel Deaconess Medical Center

Publications -  22
Citations -  1240

Abel Suárez-Fueyo is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Autoimmunity & Immune system. The author has an hindex of 13, co-authored 20 publications receiving 859 citations. Previous affiliations of Abel Suárez-Fueyo include Spanish National Research Council.

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Pathogenesis of Human Systemic Lupus Erythematosus: A Cellular Perspective

TL;DR: Novel observations have provided an improved understanding of the contribution of tissue-specific factors and associated damage, T and B lymphocytes, as well as innate immune cell subsets and their corresponding abnormalities.
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Phosphatase PP2A is requisite for the function of regulatory T cells

TL;DR: A previously unrecognized requirement for the serine-threonine phosphatase PP2A in the function of Treg cells is reported, and it is revealed that PP1A associated with components of the mTOR metabolic-checkpoint kinase pathway and suppressed the activity of themTORC1 complex.
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Grass tablet sublingual immunotherapy downregulates the TH2 cytokine response followed by regulatory T-cell generation

TL;DR: In this article, the authors evaluated the systemic effects of grass tablet allergen immunotherapy in a longitudinal analysis of humoral and cellular immune parameters in peripheral blood samples and found that grass tablet SLIT administration induced a 2-phase systemic humoral response.
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T cells in Systemic Lupus Erythematosus.

TL;DR: Systemic Lupus Erythematosus is an autoimmune disorder caused by a complex combination of genetic, epigenetic and environmental factors which result in peripheral tolerance failures and biased differentiation of T cells into pro-inflammatory and B cell-helper phenotypes.
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The CD38/NAD/SIRTUIN1/EZH2 Axis Mitigates Cytotoxic CD8 T Cell Function and Identifies Patients with SLE Prone to Infections.

TL;DR: It is proposed that high levels of CD38 lead to decreased CD8 T cell-mediated cytotoxicity and increased propensity to infections in patients with SLE, a process that can be reversed pharmacologically.