T_CELL(S)_DIFFER

Differentiation of pro-inflammatory T cell subsets in vivo

Coordinatore	INSTITUTO DE MEDICINA MOLECULAR    more Spiacenti, non ci sono informazioni su questo coordinatore. Contattare Fabio per maggiori infomrazioni, grazie.
Nazionalità Coordinatore	Portugal [PT]
Totale costo	1˙500˙000 €
EC contributo	1˙500˙000 €
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)
Code Call	ERC-2010-StG_20091118
Funding Scheme	ERC-SG
Anno di inizio	2010
Periodo (anno-mese-giorno)	2010-12-01   -   2015-11-30

 Partecipanti

#	participant	country	role	EC contrib. [€]
1	INSTITUTO DE MEDICINA MOLECULAR  Organization address address: AVENIDA PROF EGAS MONIZ city: LISBOA postcode: 1649 028 contact info Titolo: Dr. Nome: Margarida Cognome: Pinto Gago Email: send email Telefono: 351218000000 Fax: 351218000000	PT (LISBOA)	hostInstitution	1˙500˙000.00
2	INSTITUTO DE MEDICINA MOLECULAR  Organization address address: AVENIDA PROF EGAS MONIZ city: LISBOA postcode: 1649 028 contact info Titolo: Prof. Nome: Bruno Miguel De Carvalho E Silva Cognome: Santos Email: send email Telefono: 351915000000 Fax: 351218000000	PT (LISBOA)	hostInstitution	1˙500˙000.00

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 Obiettivo del progetto (Objective)

'Our understanding of T cell differentiation impacts on vaccine development and on the treatment of (auto) immune disorders. T cells are key players in inflammation, a crucial component of the immune response to pathogens that causes severe damage to the host when uncontrolled. The cytokines Interferon-(IFN-) and Interleukin-17 (IL-17) are critical mediators of the proinflammatory activity of T cells usually designated as “T helper 1” (Th1) and Th17, respectively. Here we propose to investigate the contribution of all T cell lineages - CD4 and CD8 cells, and NKT cells – to global Th1 or Th17 immune responses, using various tools including a IFN-/IL-17 double reporter mouse. Importantly, we will study Th1/ Th17 differentiation in vivo, inmodels of infection with Plasmodium berghei or Mycobacterium tuberculosis. We will analyse theindividual and combined contributions of the distinct T cell subsets, their cellular interactions andpotential interdependence in lymphoid organs and in target organs of infection. We further envisage a molecular understanding of how innate (and NKT) and adaptive (CD4 and CD8) T cell subsets acquire their respective capacities to produce IFN-or IL-17 in vivo. We will dissect (pre-/ post-) transcriptional mechanisms of regulation of Ifng and Il17 expression in the various T cell subsets, ultimately at the single-cell level. We aim at characterizing networks of transcription factors and microRNAs that regulate Th1/ Th17 differentiation either in all or in specific T cell subsets. We are particularly interested in addressing the constitutive expression of IFN-or IL-17 by innate T lymphocytes, which is set up in the thymus. We will define the molecular components of this “developmental pre-programming” of and NKT cells in comparison with the mechanisms of peripheral induction of CD4 Th1/ Th17 cell differentiation upon infection. By contrast to the generalized focus on CD4 T cells, this project will consider Th1/ Th17 differentiation of all T cell lineages and their in vivo contributions to relevant models of infection. I believe this holistic view of organism-based immune parameters and their underlying molecular mechanisms, down to the single-cell level, will significantly advance our understanding of how the Immune System works.'