Granucci-4-e1424253113191

Role: Head of Lab
Unit: Cell Signalling Innate Immunity
Hospital: Humanitas Clinical and Research Center, Italy

Role: Associate Professor of Immunology and General Pathology
University: University of Milano-Bicocca

francesca.granucci@humanitasresearch.it

SCOPUS Author ID
7004666478

 

Biographical note

Francesca Granucci received her PhD in Pharmacology and Toxicology from the University of Milan in 1996. She then performed the Post doc at the Dana Farber Cancer Institute – Boston. From 1998 to 2001 she worked as Research Associate at the CNR in Milan and from 2001 to 2006 she worked as Research Associate at the University of Milano-Bicocca. She is currently Associate Professor of Immunology and General Pathology at the Department of Biotechnology and Biosciences of the University of Milano-Bicocca and chief of the Cell Signaling and Innate Immunity Lab at the Humanitas Clinical and Reseach Center. In 2012 she obtained the EFIS-EJI Ita Askonas prize as best female group leader in immunology.

Scientific interests

Francesca Granucci has pioneered systems biology approaches to study complex dynamic processes, such as host-pathogen interactions, the process of dendritic cell maturation and the role of dendritic cells in activating and controlling NK cell functions. More recently she focused her research activity on signalling events downstream of CD14/TLR4 within cells of the mammalian innate immune system and she identified some of the key functions played by the NFATc family of transcription factors activated in phagocytes in response to PRR agonists. Very recent works indicate that in innate immune cells this pathway has a fundamental role for the development of chronic inflammatory diseases, and in controlling the crosstalk with the endothelium and with adaptive immune cells in response to microbial stimuli. The research activity of Laboratory is focused on understanding the consequences of NFAT activation in innate immune cells in models of microbial induced and sterile inflammation, such as models of acute graft rejection.

Selected publications

Zanoni I, Spreafico R, Bodio C, Cigni C, Broggi A, Gorletta T, Caccia M, Chirico G, Sironi L, Collini M, Colombo MP, Garbi N, Granucci F. “IL-15 cis-presentation is required for optimal NK Cell activation in lipopolysaccharide-mediated inflammatory conditions.” Cell Reports. Cell Rep. 2013 Sep 26;4(6):1235-49.

Vitali C, Mingozzi F, Broggi A, Barresi S, Zolezzi F, Bayry J, Raimondi G, Zanoni I, Granucci F. “Migratory, and not lymphoid-resident, dendritic cells maintain peripheral self-tolerance and prevent autoimmunity via induction of iTreg cells.” Blood. 2012 Aug 9;120(6):1237-45.

Zanoni I, Granucci F. “Regulation and dysregulation of innate immunity by NFAT signaling downstream of pattern recognition receptors (PRRs).” Eur J Immunol. 2012 Aug;42(8):1924-31.

Zanoni I, Ostuni R, Barresi S, Di Gioia M, Broggi A, Costa B, Marzi R, Granucci F. “CD14 and NFAT mediate lipopolysaccharide-induced skin edema formation in mice.” J Clin Invest. 2012 May 1;122(5):1747-57.

Zanoni I, Ostuni R, Marek LR, Barresi S, Barbalat R, Barton GM, Granucci F*, Kagan JC*. “CD14 controls the LPS-induced endocytosis of Toll-like receptor 4.” Cell. 2011 Nov 11;147(4):868-80. *equal contribution, co-corresponding

Zanoni I, Ostuni R, Capuano G, Collini M, Caccia M, Ronchi AE, Rocchetti M, Mingozzi F, Foti M, Chirico G, Costa B, Zaza A, Ricciardi-Castagnoli P, Granucci F. CD14 regulates the dendritic cell life cycle after LPS exposure through NFAT activation. Nature. 2009 Jul 9;460(7252):264-8.