TB-PATH

Novel Approaches to Determine Molecular Mechanisms of Pathogenesis in Tuberculosis

 Coordinatore  

Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.

 Nazionalità Coordinatore Non specificata
 Totale costo 1˙522˙491 €
 EC contributo 152 €
 Programma FP7-IDEAS-ERC
Specific programme: "Ideas" implementing the Seventh Framework Programme of the European Community for research, technological development and demonstration activities (2007 to 2013)
 Anno di inizio 2012
 Periodo (anno-mese-giorno) 2012-04-01   -   2017-03-31

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    MEDICAL RESEARCH COUNCIL

 Organization address address: NORTH STAR AVENUE POLARIS HOUSE
city: SWINDON
postcode: SN2 1FL

contact info
Titolo: Dr.
Nome: Anne
Cognome: O'garra
Email: send email
Telefono: 442088000000
Fax: 442088000000

UK (SWINDON) hostInstitution 1˙522˙491.41
2    MEDICAL RESEARCH COUNCIL

 Organization address address: NORTH STAR AVENUE POLARIS HOUSE
city: SWINDON
postcode: SN2 1FL

contact info
Titolo: Mr.
Nome: David
Cognome: Jones
Email: send email
Telefono: 442088000000

UK (SWINDON) hostInstitution 1˙522˙491.41

Mappa


 Word cloud

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

genes    ifn    mouse    gene    pathway    susceptible    pathogenesis    infected    strains    models    modular    mtb    inducible    mice    transcriptional    disease    tuberculosis    human    immune    blood    patients    signature    tb   

 Obiettivo del progetto (Objective)

'I initiated and developed an unbiased comprehensive study using whole genome array analysis of the transcriptome in blood of tuberculosis (TB) patients and provided global knowledge of the immune response and potential factors leading to TB pathogenesis. Using larger cohorts of TB patients and controls than previous studies, together with complementary analytical approaches of modular, pathway and gene level analysis, we identified a striking interferon (IFN)-inducible neutrophil-driven signature of active TB. This IFN-inducible gene signature correlated with extent of radiographic disease and was represented by Type I IFN as well as IFN-gamma-inducible genes. We propose to apply the knowledge obtained from our study of human TB to study in depth the potential role of Type I IFNs and Type I IFN-inducible genes in TB pathogenesis in susceptible genetic strains of mice infected with virulent Mycobacterium tuberculosis (MTb) strains. We propose to develop a modular tool to study complex transcriptional data in blood from mouse models of disease, as has been done for human disease, to allow accurate comparison of mouse models with human TB, and allow rapid analysis of the immune response at the transcriptional level to reflect pathogenesis, but also in the study of MTb-infected mice where potential pathways of pathogenesis have been perturbed. Based on our findings in human TB we propose to test the hypothesis that Type I IFN and genes induced by this pathway during TB, including Tripartite motif-containing proteins (TRIMs), are important determinants of pathogenesis. This will be achieved by their elimination or perturbation in susceptible TB models and in MTb-infected macrophages, dendritic cells, and neutrophils to define molecular mechanisms contributing to their role in TB pathogenesis.'

Altri progetti dello stesso programma (FP7-IDEAS-ERC)

APGREID (2013)

Ancient Pathogen Genomics of Re-Emerging Infectious Disease

Read More  

QUANTUMRELAX (2013)

Non Equilibrium Dynamics and Relaxation in Many Body Quantum Systems

Read More  

SPARSAM (2010)

Sparse Sampling: Theory, Algorithms and Applications

Read More