F
Fabio Re
Researcher at University of Tennessee Health Science Center
Publications - 44
Citations - 8402
Fabio Re is an academic researcher from University of Tennessee Health Science Center. The author has contributed to research in topics: Receptor & Inflammasome. The author has an hindex of 36, co-authored 44 publications receiving 8118 citations. Previous affiliations of Fabio Re include Mario Negri Institute for Pharmacological Research & Columbia University.
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Journal ArticleDOI
Modulation of granulocyte survival and programmed cell death by cytokines and bacterial products
TL;DR: Prolongation of survival may be important for the regulation of host resistance and inflammation, and may represent a crucial permissive step for certain cytokines and microbial products that activate gene expression and function in PMN.
Journal ArticleDOI
Interleukin-1 type II receptor: a decoy target for IL-1 that is regulated by IL-4
Francesco Colotta,Fabio Re,Marta Muzio,Riccardo Bertini,Nadia Polentarutti,Marina Sironi,J G Giri,Steven K. Dower,John E. Sims,Alberto Mantovani +9 more
TL;DR: Results indicate thatIL-1 acts on myelomonocytic cells through IL-1R I and that IL- 1R II inhibits IL-2 activity by acting as a decoy target for IL-0, and the existence of multiple pathways of regulation emphasizes the need for tight control of IL-
Journal ArticleDOI
Toll-like receptor 2 (TLR2) and TLR4 differentially activate human dendritic cells
Fabio Re,Jack L. Strominger +1 more
TL;DR: It is demonstrated that activation of dendritic cells by TLR2 or TLR4 agonists, although it led to comparable activation of NF-κB and mitogen-activated protein kinase (MAPK) family members, resulted in striking differences in cytokine and chemokine gene transcription, suggesting that TLR 2 andTLR4 signaling is not equivalent.
Journal ArticleDOI
Cutting Edge: Inflammasome activation by Alum and Alum’s adjuvant effect are mediated by NLRP3
TL;DR: It is shown that alum-induced secretion of IL-1β, IL-18, and IL-33 is mediated by the NLR (nucleotide-binding domain leucine-rich repeat-containing) protein NLRP3 and its adaptor ASC, but not by NLRC4, suggesting that activation of theNLRP3-inflammasome may be a common mechanism of action of particulate adjuvants.
Journal ArticleDOI
Interleukin 1 signaling occurs exclusively via the type I receptor.
John E. Sims,M A Gayle,Jennifer L. Slack,Mark R. Alderson,T A Bird,J G Giri,Francesco Colotta,Fabio Re,Alberto Mantovani,K Shanebeck +9 more
TL;DR: It is concluded that a very small number of type I receptors is sufficient to mediate all of the actions of IL-1 which are examined here and that the function of the type II receptor may not be to transduce signals.