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Lea Brys

Researcher at Vrije Universiteit Brussel

Publications -  46
Citations -  3686

Lea Brys is an academic researcher from Vrije Universiteit Brussel. The author has contributed to research in topics: Inflammation & Macrophage. The author has an hindex of 30, co-authored 46 publications receiving 3416 citations. Previous affiliations of Lea Brys include Katholieke Universiteit Leuven & Flanders Institute for Biotechnology.

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Tolerance and M2 (alternative) macrophage polarization are related processes orchestrated by p50 nuclear factor κB

TL;DR: In this paper, the p50 subunit of NF-κB was identified as a key regulator of M2-driven inflammatory reactions in vitro and in vivo, and p50-deficient mice showed exacerbated M1-driven inflammation and defective capacity to mount allergy and helminth-driven M2polarized inflammatory reactions.
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Macrophage galactose-type C-type lectins as novel markers for alternatively activated macrophages elicited by parasitic infections and allergic airway inflammation.

TL;DR: It is demonstrated that expression of the two members of the mouse macrophage galactose‐type C‐type lectin gene family (mMGL1 and mMGL2) is induced in diverse populations of aaMF, including peritoneal macrophages elicited during infection with the protozoan Trypanosoma Brucei brucei or the Helminth Taenia crassiceps and alveolar macrophAGE elicited in a mouse model of allergic
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M-CSF and GM-CSF Receptor Signaling Differentially Regulate Monocyte Maturation and Macrophage Polarization in the Tumor Microenvironment

TL;DR: The data uncover the multifaceted and opposing roles of M-CS FR and GM-CSFR signaling in governing the phenotype of macrophage subsets in tumors, and provide new insight into the mechanism of action underlying M- CSFR blockade.
Journal Article

Identification of a common gene signature for type II cytokine-associated myeloid cells elicited in vivo in different pathologic conditions. Commentary

TL;DR: In this article, comparative gene expression profiling of M1 and M2 cells, elicited in murine models of parasitic infections and cancer, yielded a common signature for in vivo-induced M2 populations independent of disease model, mouse strain, and organ source of cells.