2PM T CELL IMAGING

Molecular imaging analysis of the function of the cytoskeletal regulator DOCK2 during physiological T cell activation

 Coordinatore UNIVERSITAET BERN 

 Organization address address: Hochschulstrasse 4
city: BERN
postcode: 3012

contact info
Titolo: Ms.
Nome: Marianne
Cognome: Schori
Email: send email
Telefono: +41 31 631 4141
Fax: +41 31 631 3799

 Nazionalità Coordinatore Switzerland [CH]
 Totale costo 45˙000 €
 EC contributo 45˙000 €
 Programma FP7-PEOPLE
Specific programme "People" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Code Call FP7-PEOPLE-2010-RG
 Funding Scheme MC-ERG
 Anno di inizio 2011
 Periodo (anno-mese-giorno) 2011-03-01   -   2014-02-28

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    UNIVERSITAET BERN

 Organization address address: Hochschulstrasse 4
city: BERN
postcode: 3012

contact info
Titolo: Ms.
Nome: Marianne
Cognome: Schori
Email: send email
Telefono: +41 31 631 4141
Fax: +41 31 631 3799

CH (BERN) coordinator 45˙000.00

Mappa


 Word cloud

Esplora la "nuvola delle parole (Word Cloud) per avere un'idea di massima del progetto.

lymphoid    cells    dcs    pmhc    motility    cognate    interactions    lymphocytes    cell    binding    tissue    complexes    dock    loaded    inside    function    pm   

 Obiettivo del progetto (Objective)

'Recent experiments using twophoton microscopy (2PM) of lymphocytes interacting with dendritic cells (DCs) loaded with cognate peptide – major histocompability complexes (pMHC) have uncovered their dynamic interactions inside lymphoid tissue of small rodents. Depending on the amount of pMHC on the DC surface, motile T cells may either slowly integrate T cell receptor-mediated signals or immediately undergo long-term interactions with DCs. Thus, motility and T cell activation inside lymphoid tissue are closely intertwined. A key motility-inducing factor is the Rac guanine exchange factor DOCK2. Using 2PM of lymphoid tissue, we previously demonstrated that lymphocytes lacking DOCK2 showed reduced motility. However, it is unclear which intracellular binding partners regulate DOCK2 function in lymphoid cells. Furthermore, the role of DOCK2 expression during interactions between T cells and DCs displaying varying densities of cognate pMHC complexes in vivo has not been explored to date. Here, we propose to carry out an analysis of potential binding partners of DOCK2 recently identified in a yeast-two-hybrid screen. Furthermore, we will perform a 2PM analysis comparing the interaction dynamics of control and DOCK2-deficient T cells with DCs loaded with increasing amounts of cognate pMHC complexes. Our project thus aims to clarify the physiological function of DOCK2 for T cell biology.'

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