NKT CELLS IN MUCOSA

"NKT cells, CD1 expression and lipid presentation in intestinal immunity"

 Coordinatore KING'S COLLEGE LONDON 

 Organization address address: Strand
city: LONDON
postcode: WC2R 2LS

contact info
Titolo: Mr.
Nome: Paul
Cognome: Labbett
Email: send email
Telefono: 442078000000
Fax: +4420 7848 3193

 Nazionalità Coordinatore United Kingdom [UK]
 Totale costo 221˙606 €
 EC contributo 221˙606 €
 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-2013-IEF
 Funding Scheme MC-IEF
 Anno di inizio 2014
 Periodo (anno-mese-giorno) 2014-03-01   -   2016-02-29

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    KING'S COLLEGE LONDON

 Organization address address: Strand
city: LONDON
postcode: WC2R 2LS

contact info
Titolo: Mr.
Nome: Paul
Cognome: Labbett
Email: send email
Telefono: 442078000000
Fax: +4420 7848 3193

UK (LONDON) coordinator 221˙606.40

Mappa


 Word cloud

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

cell    immunity    microbial    nkt    mechanisms    diseases    cells    homeostasis    intestinal    cd    disease    lipid    immune    inflammatory    mucosal   

 Obiettivo del progetto (Objective)

'The mammalian intestine is colonized by trillions of microorganisms that are critical for the establishment of tissue homeostasis. Consequently, the immune system has developed strategies to maintain a mutualistic relation with the microbiota while stopping microbial spread. However, inappropriate function of the immune cells and/or alteration of the commensal composition can lead to inflammatory and autoimmune diseases, like inflammatory bowel disease. Among the components of the intestinal immune system, NKT cells represent a predominant population with striking immune-modulatory properties. NKT cells specifically recognize and are activated by lipid antigens presented by the MHC-I-like molecule CD1. Upon antigen encounter NKT cells can induce the downstream activation of both innate (NK cells) and adaptive (B cells) immune cells. In line with the abundance and diversity of microbial-derived lipids present in the gut, numerous studies have proposed a role for NKT cells and CD1-lipid presentation in the modulation of mucosal immunity both in homeostasis and disease. However, the features of intestinal NKT cells and the mechanisms by which they exert their immunomodulatory functions remain poorly explored. This proposal aims to unravel the cellular and molecular mechanisms that mediate the role of NKT cells in the regulation of mucosal immunity. We will use a combination of flow-cytometry, immunofluorescence and microscopy to build a comprehensive picture of NKT cell distribution and phenotype within gastro-intestinal compartments. With this established we will analyse the role of NKT cells in intestinal homeostasis by deciphering their contribution to the generation and quality of intestinal B cell responses. These studies will provide a better understanding of the factors that modulate intestinal immunity, with the potential to improve therapies for patients suffering from intestinal inflammatory diseases and possibly a broader range of disorders.'

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