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Chloé Abels
Researcher at Vrije Universiteit Brussel
Publications - 10
Citations - 852
Chloé Abels is an academic researcher from Vrije Universiteit Brussel. The author has contributed to research in topics: Liver injury & Tumor microenvironment. The author has an hindex of 6, co-authored 9 publications receiving 643 citations. Previous affiliations of Chloé Abels include Flanders Institute for Biotechnology.
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Journal ArticleDOI
Bone marrow-derived monocytes give rise to self-renewing and fully differentiated Kupffer cells
Charlotte L. Scott,Fang Zheng,Fang Zheng,Patrick De Baetselier,Liesbet Martens,Yvan Saeys,Sofie De Prijck,Saskia Lippens,Chloé Abels,Steve Schoonooghe,Geert Raes,Nick Devoogdt,Bart N. Lambrecht,Alain Beschin,Martin Guilliams +14 more
TL;DR: It is shown that circulating monocytes engraft in the liver, gradually adopt the transcriptional profile of their depleted counterparts and become long-lived self-renewing cells, like embryonic precursors if the niche is available to them.
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M-CSF and GM-CSF Receptor Signaling Differentially Regulate Monocyte Maturation and Macrophage Polarization in the Tumor Microenvironment
Eva Van Overmeire,Benoit Stijlemans,Felix Heymann,Jiri Keirsse,Yannick Morias,Yvon Elkrim,Lea Brys,Chloé Abels,Qods Lahmar,Can Ergen,Lars Vereecke,Frank Tacke,Patrick De Baetselier,Jo A. Van Ginderachter,Damya Laoui +14 more
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.
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Ly6C- Monocytes Regulate Parasite-Induced Liver Inflammation by Inducing the Differentiation of Pathogenic Ly6C+ Monocytes into Macrophages.
Yannick Morias,Chloé Abels,Damya Laoui,Eva Van Overmeire,Martin Guilliams,Elio Schouppe,Frank Tacke,Carlie J. deVries,Patrick De Baetselier,Alain Beschin +9 more
TL;DR: Ly6C– monocytes can dampen liver damage caused by an extensive Ly6C+ monocyte-associated inflammatory immune response in T. congolense trypanotolerant animals, and may represent a therapeutic approach in liver pathogenicity induced by chronic infection.
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Involvement of connexin43 in acetaminophen-induced liver injury
Michaël Maes,Mitchell R. McGill,Tereza Cristina da Silva,Chloé Abels,Margitta Lebofsky,Cintia Maria Monteiro de Araújo,Taynã Tiburcio,Isabel Veloso Alves Pereira,Joost Willebrords,Sara Crespo Yanguas,Anwar Farhood,Alain Beschin,Jo A. Van Ginderachter,Maria Lúcia Zaidan Dagli,Hartmut Jaeschke,Bruno Cogliati,Mathieu Vinken +16 more
TL;DR: It was found that gap junction communication deteriorates upon acetaminophen intoxication in wild type mice, which is associated with a switch in mRNA and protein production from connexin32 andConnexin26 to connexIn43, which suggests that hepatic connex in43-based signaling may protect against acetamophen-induced liver toxicity.
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Monitoring liver macrophages using nanobodies targeting Vsig4: concanavalin A induced acute hepatitis as paradigm.
Fang Zheng,Nick Devoogdt,Amanda Sparkes,Yannick Morias,Chloé Abels,Benoit Stijlemans,Tony Lahoutte,Serge Muyldermans,Patrick De Baetselier,Steve Schoonooghe,Alain Beschin,Geert Raes +11 more
TL;DR: Results indicate that Nbs targeting Vsig4 as molecular imaging biomarker enable non-invasive monitoring of KCs during hepatic inflammation.