General Info

Rossi Paccani Silvia - Technician/Tecnico

Email: rossipaccan2@unisi.it

Office/Ufficio: +39 (0)577 234403

Laboratory/Laboratorio: +39 (0)577 234396

Fax: +39 (0)577 234476

Skype: -

Research Group

Nico Giommoni, Nagaja Capitani, Orso Maria Lucherini, Cosima Tatiana Baldari, Silvia Rossi Paccani, Francesca Finetti, Laura Patrussi, Giulia Masi, Cristina Ulivieri, Daniela Fanigliulo, Maria Teresa Savino, Micol Ferro

Research Interest

The activity of the lab is focused on the functional dissection of signal transduction pathways in lymphocyte activation and apoptosis and dysregulation of these processes un lymphoproliferative, immunodeficiency and pathogen-related diseases.

Current research topics include:

* Characterization of the Shc family of protein adapters in the immune system
* Modulation of antigen receptor signaling by bacterial toxins as a strategy of immune evasion
* Regulation of membrane trafficking at the immune synapse by the intraflagellar transport system

Curriculum Vitae

Date of birth: February 10, 1974
Place of birth: Siena, Italy

University Education
2000     Degree with honours in Biological Sciences, Faculty of Mathematical, Physical and Natural     Sciences, University of Siena. Experimental thesis work in Molecular biology under the     supervision of Prof. Cosima T. Baldari
2002    Master in Evolutionary Biology Dept. Evolutionary Biology, University of Siena
2001-2004 PhD studentship in Evolutionary Biology, University of Siena
2005    PhD in Evolutionary Biology

Scientific activity
2000-2002: Research fellow Dept. Evolutionary Biology, Univ. Siena  (group Prof C.T. Baldari).
Research focus: Biochemical and genetic characterization of T cells from common variable immunoeficiency patients (CVID) and study of the regulation of stress activated kinases in T cells.
2002-present: Staff scientist, Dept. Evolutionary Biology, Univ. Siena (group Prof C.T. Baldari).
Research focus: Signaling in the immune system in health and disease. Study of antigen receptor and chemokine receptor signaling in T cells and dysregulation of these processes both by drugs (NSAIDs) and by bacterial pathogens (H. pylori, B. anthracis and B. pertussis)

Teaching experience
2009/2010 Contract professor, Molecular Biology, Faculty of Sciences, Univ. Siena
2008/2009 Contract professor, Lab course of Molecular Biology, Faculty of Sciences, Univ. Siena 2007/2008 Contract professor, Lab course of Molecular Biology, Faculty of Sciences, Univ. Siena 2006/2007 Contract professor, Lab course of Molecular Biology, Faculty of Sciences, Univ. Siena
2005/2006 Contract professor, Course of Molecular Biology, Faculty of Sciences, Univ. Siena
2004/2005 Contract professor, Course of Molecular Biology, Faculty of Sciences, Univ. Siena
2001/2002 Instructor, Course of Experimental Biology I and II Faculty of Sciences, Faculty of Sciences, Univ. Siena

Selected Publications

Silvia Rossi Paccani, Francesca Finetti, Marilyne Davi, Laura Patrussi, Daniel Ladant, Cosima T Baldari The Bordetella pertussis adenylate cyclase toxin binds to T cells via LFA-1 and induces its release from the immune synapse (JEM 2010, submitted)

Silvia Rossi Paccani, Marisa Benagiano, Maria Teresa Savino, Fiorella Tonello, Mario M. D’Elios, MD, Cosima T. Baldari, The adenylate cyclase toxin of Bacillus anthracis is a potent promoter of Th17 cell differentiation. (J Allergy Clin Immunol 2010, submitted)

Finetti F, Paccani SR, Riparbelli MG, Giacomello E, Perinetti G, Pazour GJ, Rosenbaum JL, Baldari CT. Intraflagellar transport is required for polarized recycling of the TCR/CD3 complex to the immune synapse. Nat Cell Biol. 2009 Nov;11(11):1332-9. Epub 2009 Oct 25. PubMed PMID: 19855387; PubMed Central PMCID:PMC2837911.

Tournier JN, Rossi Paccani S, Quesnel-Hellmann A, Baldari CT. Anthrax toxins: a weapon a weapon to systematically dismantle the host immune defenses. Mol Aspects Med. 2009 Dec;30(6):456-66. Epub 2009 Jun 26. Review. PubMed PMID: 19560486.


Paccani SR, M. Benagiano, N. Capitani, I. Zornetta, D. Ladant, C. Montecucco, M. M. D'Elios, C. T. Baldari The adenylate cyclase toxins of Bacillus anthracis and Bordetella pertussis promote Th2 cell development by shaping T cell antigen receptor signalling PLoS Pathogens 2009,Mar;5(3):e1000325.

Paccani SR, Dal Molin F, Benagiano M, Ladant D, D'Elios MM, Montecucco C, Baldari CT. Suppression of T-lymphocyte activation and chemotaxis by the adenylate cyclise toxin of Bordetella pertussis. Infect Immun. 2008;76(7):2822-32.

Rossi Paccani S, Tonello F, Patrussi L, Capitani N, Simonato M, Montecucco C, Baldari CT. Anthrax toxins inhibit immune cell chemotaxis by perturbing chemokine receptor signalling. Cell Microbiol. 2007;9(4):924-9.

Paccani SR, Boncristiano M, Patrussi L, Ulivieri C, Wack A, Valensin S, Hirst TR, Amedei A, Del Prete G, Telford JL, D'Elios MM, Baldari CT. Defective Vav expression and impaired F-actin reorganization in a subset of patients with common variable immunodeficiency characterized by T-cell defects. Blood.2005, 106(2):626-34

Paccani SR, Tonello F, Ghittoni R, Natale M, Muraro L, D'Elios MM, Tang WJ, Montecucco C, Baldari CT. Anthrax toxins suppress T lymphocyte activation by disrupting antigen receptor signaling. J Exp Med. 2005;201(3):325-31.

Paccani SR, Patrussi L, Ulivieri C, Masferrer JL, D'Elios MM, Baldari CT. Nonsteroidal anti-inflammatory drugs inhibit a Fyn-dependent pathway coupled to Rac and stress kinase activation in TCR signaling. Blood.2005, 105(5):2042-8.

Boncristiano M., Rossi Paccani S., Barone S., Ulivieri C., Patrussi L., D’Elios M.M., Telford J. L e Baldari C.T. The Helicobacter pilori vacuolating toxin inhibits T-cell activation by two indipendent mechanisms. J. Exp. Med. 2003, 198: 1887-1897.