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Regulation of lipid-mediated immunity in the intestine

Total Cost €


EC-Contrib. €






Project "LIPID IMMUNITY" data sheet

The following table provides information about the project.


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

contact info
title: n.a.
name: n.a.
surname: n.a.
function: n.a.
email: n.a.
telephone: n.a.
fax: n.a.

 Coordinator Country United Kingdom [UK]
 Project website
 Total cost 195˙454 €
 EC max contribution 195˙454 € (100%)
 Programme 1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
 Code Call H2020-MSCA-IF-2015
 Funding Scheme MSCA-IF-EF-ST
 Starting year 2016
 Duration (year-month-day) from 2016-03-01   to  2018-02-28


Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    KING'S COLLEGE LONDON UK (LONDON) coordinator 195˙454.00


 Project objective

The gastrointestinal tract is continuously exposed to multiple antigens from commensal bacteria, food and pathogens. The mechanisms by which the gut mucosa tolerates trillions of commensal bacteria without developing inflammation remains poorly understood. It is increasingly appreciated that commensal bacteria-derived products regulate the homeostasis and/or function of many immune cell populations. Commensal bacteria-derived lipids are recognized by a population of unconventional T cells, called NKT cells. NKT cells specifically recognize through their T cell receptor lipid antigens presented by the MHC-I-like molecule CD1 which is expressed by a variety of immune cells within the intestinal tissue. Importantly, commensal-derived lipids modulate the numbers, phenotype and function of intestinal NKT cells. Conversely, dysregulation of NKT cell activation and/or CD1 expression have been associated with the development of colitis in mice and humans. Despite the abundance and diversity of microbial-derived lipids present in the gut, the molecular and cellular mechanisms that mediate their recognition by immune cells and the identity of the antigen presenting cells involved in this process remain unknown. By using a combination of multiparametric flow cytometry, genetic engineering and in vivo experiments this proposal aims to unravel the mechanisms and functional consequences of lipid-presentation in the mucosa. 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.


year authors and title journal last update
List of publications.
2018 Julia Sáez de Guinoa, Rebeca Jimeno, Mauro Gaya, David Kipling, María José Garzón, Deborah Dunn‐Walters, Carles Ubeda, Patricia Barral
CD1d‐mediated lipid presentation by CD11c + cells regulates intestinal homeostasis
published pages: e97537, ISSN: 0261-4189, DOI: 10.15252/embj.201797537
The EMBO Journal 37/5 2019-06-13
2016 Julia Saez de Guinoa, Rebeca Jimeno, Nazanin Farhadi, Peter J Jervis, Liam R Cox, Gurdyal S Besra, Patricia Barral
CD1d‐mediated activation of group 3 innate lymphoid cells drives IL‐22 production
published pages: e201642412, ISSN: 1469-221X, DOI: 10.15252/embr.201642412
EMBO reports 2019-06-13

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