Laura Patrussi

Prof. Laura Patrussi

Department of Life Sciences, University of Siena
orcid

Research Focus & Metrics

Academic Career Length

25Years (2002-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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15 December 2003 in Journal of Experimental Medicine
Verified
Journal Article
Open access
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MBMarianna Boncristiano
Marianna Boncristiano
SPSilvia Rossi Paccani
Silvia Rossi Paccani
SBSilvia Barone
Silvia Barone
Cristina UlivieriCristina Ulivieri
Cristina Ulivieri
Laura PatrussiLaura Patrussi
Laura Patrussi
CBCosima T. Baldari
Cosima T. Baldari
Helicobacter pylori toxin, VacA, damages the gastric epithelium by erosion and loosening of tight junctions. Here we report that VacA also interferes with T cell activation by two different mechanisms. Formation of anion-specific channels by VacA prevents calcium influx from the extracellular milieu. The transcription factor NF-AT thus fails to translocate to the nucleus and activate key cytokine genes. A second, channel-independent mechanism involves activation of intracellular signaling through the mitogen-activated protein kinases MKK3/6 and p38 and the Rac-specific nucleotide exchange factor, Vav. As a consequence of aberrant Rac activation, disordered actin polymerization is stimulated. The resulting defects in T cell activation may help H. pylori to prevent an effective immune response leading to chronic colonization of its gastric niche.

1 February 2004 in Molecular and Cellular Biology
Verified
Journal Article
Closed access
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SPSonia Pacini
Sonia Pacini
MPMichela Pellegrini
Michela Pellegrini
EMEnrica Migliaccio
Enrica Migliaccio
Laura PatrussiLaura Patrussi
Laura Patrussi
Cristina UlivieriCristina Ulivieri
Cristina Ulivieri
CBCosima T. Baldari
Cosima T. Baldari
Of the three Shc isoforms, p66Shc is responsible for fine-tuning p52/p46Shc signaling to Ras and has been implicated in apoptotic responses to oxidative stress. Here we show that human peripheral blood lymphocytes and mouse thymocytes and splenic T cells acquire the capacity to express p66Shc in response to apoptogenic stimulation. Using a panel of T-cell transfectants and p66Shc−/− T cells, we show that p66Shc expression results in increased susceptibility to apoptogenic stimuli, which depends on Ser36 phosphorylation and correlates with an altered balance in apoptosis-regulating gene expression. Furthermore, p66Shc blunts mitogenic responses to T-cell receptor engagement, at least in part by transdominant inhibition of p52Shc signaling to Ras/mitogen-activated protein kinases, in an S36-dependent manner. The data highlight a novel interplay between p66Shc and p52Shc in the control of T-cell fate.

27 January 2005 in The FASEB Journal
Verified
Journal Article
Closed access
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RGRaffaella Ghittoni
Raffaella Ghittoni
Laura PatrussiLaura Patrussi
Laura Patrussi
KPKatja Pirozzi
Katja Pirozzi
MPMichela Pellegrini
Michela Pellegrini
PLPietro E. Lazzerini
Pietro E. Lazzerini
CBCosima T. Baldari
Cosima T. Baldari

1 January 2014 in Journal of Cell Science
Verified
Journal Article
Open access
PDF file
FFFrancesca Finetti
Francesca Finetti
Laura PatrussiLaura Patrussi
Laura Patrussi
GMGiulia Masi
Giulia Masi
AOAnna Onnis
Anna Onnis
DGDonatella Galgano
Donatella Galgano
CBCosima T. Baldari
Cosima T. Baldari
T cell activation requires sustained signaling at the immune synapse, a specialized interface with the antigen-presenting cell (APC) that assembles following T cell antigen receptor (TCR) engagement by major histocompatibility complex (MHC)-bound peptide. Central to sustained signaling is the continuous recruitment of TCRs to the immune synapse. These TCRs are partly mobilized from an endosomal pool by polarized recycling. We have identified IFT20, a component of the intraflagellar transport (IFT) system that controls ciliogenesis, as a central regulator of TCR recycling to the immune synapse. Here, we have investigated the interplay of IFT20 with the Rab GTPase network that controls recycling. We found that IFT20 forms a complex with Rab5 and the TCR on early endosomes. IFT20 knockdown (IFT20KD) resulted in a block in the recycling pathway, leading to a build-up of recycling TCRs in Rab5+ endosomes. Recycling of the transferrin receptor (TfR), but not of CXCR4, was disrupted by IFT20 deficiency. The IFT components IFT52 and IFT57 were found to act together with IFT20 to regulate TCR and TfR recycling. The results provide novel insights into the mechanisms that control TCR recycling and immune synapse assembly, and underscore the trafficking-related function of the IFT system beyond ciliogenesis.

13 March 2015 in Cell Death & Differentiation
Verified
Journal Article
Closed access
AOAnna Onnis
Anna Onnis
FFFrancesca Finetti
Francesca Finetti
Laura PatrussiLaura Patrussi
Laura Patrussi
MGM Gottardo
M Gottardo
CCChiara Cassioli
Chiara Cassioli
CBCosima T. Baldari
Cosima T. Baldari

1 February 2002 in European Journal of Immunology
Verified
Journal Article
Closed access
PDF file
SVSilvia Valensin
Silvia Valensin
SPSilvia Rossi Paccani
Silvia Rossi Paccani
CUCristina Ulivieri
Cristina Ulivieri
DMDavid Mercati
David Mercati
SPSonia Pacini
Sonia Pacini
CBCosima T. Baldari
Cosima T. Baldari