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Alberto Mantovani, MD
Professor
University of Milan
Scientific Director
Istituto Clinico Humanitas
Alberto Mantovani was born in Milan in 1948. He graduated (summa cum laude) in 1973 in Medicine
at the University of Milan and in 1976 he specialized in Oncology at the University of Pavia.
From 1973 to 1975 he had a scholarship at the Laboratory of Immunology and Chemotherapy at the
Mario negri Institute in Milano. From 1973 to 1976 he was visiting fellow at the Department of
Tumor Immunology of the Chester Research Institute in Belmont (GB). In 1978-1979 he was visiting
fellow at the Laboratory of Immunodiagnosis, NIH, Bethesda (USA), with a
Yamagiwa-Yoshida Scholarship of the UICC first and then with a NATO grant.
From 1979 to 1981 he was Senior investigator, Department of Tumor Immunology
and Chemotherapy, Istituto di Ricerche Farmacologiche "Mario Negri", Milan. In 1981 he became
Chief of the Laboratory of Immunology, Istituto di Ricerche Farmacologiche "Mario Negri". From 1994
to 2001 he was full Professor of General Pathology, School of Medicine, University of Brescia,
Italy.
From 1996 to 2005 he has lead the Department of Immunology and Cell Biology at the Istituto
di Ricerche Farmacologiche "Mario Negri", Milan.
Since 2001 he is full Professor of General Pathology, School of Medicine, State University of
Milan.
Since October 2005 he is Scientific Director of Istituto Clinico Humanitas, Milan, Italy and
President and founder of the Fondazione Humanitas per la Ricerca.
In 1998 he won the Biotec award (Dompè); in 2000 he won the T.Bonazinga Award, SLB (Cambridge,
MA, USA). In 2004 he was awarded the Guido Venosta Prize by the President of the Republic of Italy.
Since 2000 is a member of the European Molecular Biology Organization (EMBO) and since 2002 he is a
member of the Henry Kunkel Society. On Sept. 2005 he has been elected Councilor of the
International Cytokine Society.
His research centers mainly on molecular regulation mechanisms of leukocyte infiltration. More
specifically his attention is focused on the molecular function and regulation circuits of the
inflammatory cytokines. The first interest was the primary inflammatory cytokine interleukin 1
(IL-1). In particular negative regulation circuits made up of type II decoy receptors. This
molecule, membrane bound or released, acts as a molecular trap for the IL-1, constituting a unique
system in biology. This paradigm was subsequently generalized by other inflammatory cytokines. In
addition, a new IL-1 antagonist receptor was identified and defined.
In general these studies bring to light the complexity and uniqueness of IL-1 negative
regulation mechanisms.
A second line of work centers on the study of secondary cytokines known as chemokines. New
molecules have been defined (for example, macrophage derived chemokines, MDC) and new cellular
targets. Among these the study of dendrite and endothelial cells has been emphasized.
In addition, the discovery that pro- and anti- inflammatory signals not only regulate the level
of chemokine production but also the level of receptions offers a new level of understanding of how
the system functions and possible targets for therapeutic interventions. Finally, his group has
cloned the PTX3 (cDNA and genome, human and mouse), the first member of the long pentraxin family,
and defined his function in innate immunity and inflammation. |