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Sergio Bernasconi

Researcher at Mario Negri Institute for Pharmacological Research

Publications -  121
Citations -  7946

Sergio Bernasconi is an academic researcher from Mario Negri Institute for Pharmacological Research. The author has contributed to research in topics: Cell adhesion molecule & Monocyte. The author has an hindex of 45, co-authored 113 publications receiving 7703 citations. Previous affiliations of Sergio Bernasconi include University of Brescia & University of Trieste.

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Journal ArticleDOI

Regulation of the chemokine receptor CXCR4 by hypoxia.

TL;DR: It is described that oxygen availability is a determinant parameter in the setting of chemotactic responsiveness to stromal-derived factor 1 (CXCL12), and the Hyp–Hyp-inducible factor 1 α–CXCR4 pathway may regulate trafficking in and out of hypoxic tissue microenvironments.
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Biologic response of B lymphoma cells to anti-CD20 monoclonal antibody rituximab in vitro: CD55 and CD59 regulate complement-mediated cell lysis

TL;DR: It is concluded that CDC and ADCC are major mechanisms of action of rituximab on B-cell lymphomas and that a heterogeneous susceptibility of different lymphoma cells to complement may be at least in part responsible for the heterogeneity of the response of different patients to ritUXimab in vivo.
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CD20 levels determine the in vitro susceptibility to rituximab and complement of B-cell chronic lymphocytic leukemia: further regulation by CD55 and CD59

TL;DR: Data demonstrate that CD20, CD55, and CD59 are important factors determining the in vitro response to rituximab and complement and indicate potential strategies to improve the clinical response to this biologic therapy.
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Expression of adhesion molecules and chemotactic cytokines in cultured human mesothelial cells.

TL;DR: Results indicate that mesothelial cells can express a set of adhesion molecules and chemotactic cytokines overlapping with, but distinct from, that expressed in vascular endothelium, and that these are functionally relevant for interacting with mononuclear phagocytes.