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Prof. Maria Laura Belladonna
Department of Medicine and Surgery, University of Perugia, Italy
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Academic Career Length
35Years (1992-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications26 October 2003 in Nature Immunology
Journal Article
Francesca FallarinoUGUrsula Grohmann
Ursula GrohmannKHKwang Woo Hwang
Kwang Woo Hwang
COCiriana Orabona
Ciriana OrabonaCVCarmine Vacca
Carmine Vacca
Paolo Puccetti +4
30 September 2002 in Nature Immunology
Journal Article
UGUrsula Grohmann
Ursula GrohmannCOCiriana Orabona
Ciriana OrabonaFrancesca FallarinoCVCarmine Vacca
Carmine VaccaFCFilippo Calcinaro
Filippo Calcinaro
Paolo Puccetti +5
1 June 2006 in The Journal of Immunology
Journal Article
Francesca FallarinoUGUrsula Grohmann
Ursula GrohmannSYSylvaine You
Sylvaine YouBMBarbara C. McGrath
Barbara C. McGrath
DCDouglas R. Cavener
Douglas R. Cavener
Paolo Puccetti +7
Tryptophan catabolism is a tolerogenic effector system in regulatory T cell function, yet the general mechanisms whereby tryptophan catabolism affects T cell responses remain unclear. We provide evidence that the short-term, combined effects of tryptophan deprivation and tryptophan catabolites result in GCN2 kinase-dependent down-regulation of the TCR ζ-chain in murine CD8+ T cells. TCR ζ down-regulation can be demonstrated in vivo and is associated with an impaired cytotoxic effector function in vitro. The longer-term effects of tryptophan catabolism include the emergence of a regulatory phenotype in naive CD4+CD25− T cells via TGF-β induction of the forkhead transcription factor Foxp3. Such converted cells appear to be CD25+, CD69−, CD45RBlow, CD62L+, CTLA-4+, BTLAlow and GITR+, and are capable of effective control of diabetogenic T cells when transferred in vivo. Thus, both tryptophan starvation and tryptophan catabolites contribute to establishing a regulatory environment affecting CD8+ as well as CD4+ T cell function, and not only is tryptophan catabolism an effector mechanism of tolerance, but it also results in GCN2-dependent generation of autoimmune-preventive regulatory T cells.
9 July 2014 in Nature
Journal Article
ABAlban Bessede
Alban Bessede
Marco GargaroMPMaria Teresa Pallotta
Maria Teresa PallottaDMDavide Matino
Davide MatinoGSGiuseppe Servillo
Giuseppe ServilloPaolo Puccetti +32
31 July 2011 in Nature Immunology
Journal Article
MPMaria Teresa Pallotta
Maria Teresa PallottaCOCiriana Orabona
Ciriana OrabonaCVClaudia Volpi
Claudia VolpiCVCarmine Vacca
Carmine VaccaMBMaria Laura Belladonna
Maria Laura BelladonnaUGUrsula Grohmann
Ursula Grohmann +11
26 September 2007 in European Journal of Immunology
Journal Article
TERESA ZELANTEALAntonella De Luca
Antonella De LucaPBPierluigi Bonifazi
Pierluigi Bonifazi
CMClaudia Montagnoli
Claudia Montagnoli
SBSilvia Bozza
Silvia Bozza
LRLuigina Romani
Luigina Romani +9
Although inflammation is an essential component of the protective response to fungi, its dysregulation may significantly worsen fungal diseases. We found here that the IL‐23/IL‐17 developmental pathway acted as a negative regulator of the Th1‐mediated immune resistance to fungi and played an inflammatory role previously attributed to uncontrolled Th1 cell responses. Both inflammation and infection were exacerbated by a heightened Th17 response against Candida albicans and Aspergillus fumigatus, two major human fungal pathogens. IL‐23 acted as a molecular connection between uncontrolled fungal growth and inflammation, being produced by dendritic cells in response to a high fungal burden and counter‐regulating IL‐12p70 production. Both IL‐23 and IL‐17 subverted the inflammatory program of neutrophils, which resulted in severe tissue inflammatory pathology associated with infection. Our data are the first demonstrating that the IL‐23/IL‐17 pathway promotes inflammation and susceptibility in an infectious disease model. As IL‐23‐driven inflammation promotes infection and impairs antifungal resistance, modulation of the inflammatory response represents a potential strategy to stimulate protective immune responses to fungi.See accompanying commentary: http://dx.doi.org/10.1002/eji.200737804
About Me
Maria Laura Belladonna is a professor of Biology at the University of Perugia, ItalyProf. Belladonna is a biologist with a background in immunopharmacology. After graduating with honors in Drug Chemistry and Technology at the University of Perugia in 1996, she obtained her PhD degree in Experimental Medicine, discussing a thesis on the immunogenicity acquired by drug-treated tumor antigens. After her PhD, she was a research fellow under the supervision of Dr. JC Renauld at the Ludwig Institute for Cancer Research in Brussels, where she acquired significant expertise in the production of recombinant heterodimeric cytokines and the analysis of their signaling. Now, her research activity is carried out at the Pharmacology Section of the Department of Medicine and Surgery (University of Perugia, Italy). Her research field is the in vitro study of molecular mechanisms of immunogenic and tolerogenic responses, effects of tolerogenic cytokines, the tolerogenic enzyme indoleamine 2,3-dioxygenase 1 (IDO1), and tryptophan metabolism in murine experimental models of autoimmune diseases and tumors, tumor biomarkers derived from tryptophan metabolism in human Non-Small Cell Lung Cancer (NSCLC), the effects of plant-derived bioactive compounds in the regulation of osteoclastogenesis, and the effects of oxidative stress molecules in bone-damaging diseases. She is a member of the AIBG (Associazione Italiana di Biologia e Genetica) and SIF (Società Italiana Farmacologia) scientific societies.