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Maria Grazia Uguccioni
Institute for Research in Biomedicine, Bellinzona, Switzerland
Education and Academic Background
Faculty of Medicine and Surgery, University of Bologna, Italy
Specialization in Hematology, University of Bologna, Italy
- 1998-2000 Chair 7th workshop on Human Leukocyte Differentiation Antigens (cytokine-chemokine receptor section)
- 2000-2004 Chair 8th workshop on Human Leukocyte Differentiation Antigens (cytokine-chemokine receptor section)
- 1999-2004 Adjunct Professor, School of Toxicology, Faculty of Pharmacology, University of Bologna, Italy
- 2006-2011 Adjunct Professor, School of Rheumatology, Faculty of Medicine, University of Bologna, Italy
Scientific and Research Interests
The research interest of my group remains focused on Chemokine activities in physiology and pathology, with an emphasis on the mechanisms governing fine-tuning modulation of their expression and activity. Chemokines are secreted proteins and have emerged as key controllers of integrin function and cell locomotion. The effects of chemokines are mediated by seven transmembrane domain receptors coupled to GTP-binding proteins, which are differentially expressed in a wide range of cell types. The resulting combinatorial diversity in responsiveness to chemokines guarantees the proper tissue distribution of distinct leukocyte subsets under normal and inflammatory/pathological conditions. A vast range of in situ experiments, aimed at understanding which chemokines are produced in specific circumstances, has revealed that a variety of chemokines can be concomitantly produced at target sites of leukocyte trafficking and homing. This renders the chemokine system a good target for therapy, and has increased the search by pharmaceutical companies for small molecule chemokine antagonists. While we understand the effects of different chemokines individually, much less is known about the potential consequences of the expression of multiple chemokines, cytokines, toll-like receptor ligands or other inflammatory molecules on leukocyte migration and function. Our group discovered the existence of additional features of chemokines: their ability to antagonize or enhance, as synergy-inducing chemokines, the activity of other chemokines.
- Cecchinato V., Bernasconi E., Speck R.F., Proietti M., Sauermann U., D’Agostino G., Danelon G., Rezzonico Jost T., Grassi F., Raeli L., Schöni-Affolter F., Stahl-Hennig C., Uguccioni M., and the Swiss HIV Cohort Study. Impairment of CCR6+ and CXCR3+ T-helper cell migration in HIV-1 infection is rescued by modulating actin polymerization. J. Immunol. 2017, 198:184-195.
- Proudfoot A., and Uguccioni M. Modulation of chemokine responses: synergy and cooperativity. Frontiers in Immunology 2016, 7:183.
- Cecchinato V., D’Agostino G., Raeli L., and Uguccioni M. Fine tuning modulation of chemokine activities induced by synergy-inducing molecules. Leukoc. Biol. 2016, 99:851-855.
- Venereau E., Casalgrandi M., Schiraldi M., Antoine D.J., Cattaneo A., De Marchis F., Liu J., Antonelli A., Preti A., Raeli L., Shams S.S., Yang H., Varani L., Andersson U., Tracey K. J., Bachi A., Uguccioni M. and Bianchi M.E. Mutually exclusive redox forms of HMGB1 promote cell recruitment or proinflammatory cytokine release. J Exp Med 2012; 209:1519-1528.
- Schiraldi M., Raucci A., Livoti E., Apuzzo T., De Marchis F., Celona B., Pedotti M., Thelen M., Varani L., Proudfoot A., Bianchi M.E. and Uguccioni M. The alarmin HMGB1 promotes recruitment of inflammatory cells to damaged tissues by binding CXCL12 and signaling via CXCR4. J Exp Med 2012; 209:551-563.
Academic honors, awards and prices
Member of the Academy of Science of the Institute of Bologna (http://www.accademiascienzebologna.it/en).