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NANOBreg SIGNED

A new therapeutic platform based on nanotechnology to promote T- and B-regulatory networks

Total Cost €

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EC-Contrib. €

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Partnership

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 NANOBreg project word cloud

Explore the words cloud of the NANOBreg project. It provides you a very rough idea of what is the project "NANOBreg" about.

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Project "NANOBreg" data sheet

The following table provides information about the project.

Coordinator
CONSORCI INSTITUT D'INVESTIGACIONS BIOMEDIQUES AUGUST PI I SUNYER 

Organization address
address: CALLE ROSSELLO 149 PUERTA BJS
city: BARCELONA
postcode: 8036
website: http://www.idibaps.org/en_index.html

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 Spain [ES]
 Project website http://www.idibaps.org
 Total cost 158˙121 €
 EC max contribution 158˙121 € (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-RI
 Starting year 2016
 Duration (year-month-day) from 2016-05-01   to  2018-05-13

 Partnership

Take a look of project's partnership.

# participants  country  role  EC contrib. [€] 
1    CONSORCI INSTITUT D'INVESTIGACIONS BIOMEDIQUES AUGUST PI I SUNYER ES (BARCELONA) coordinator 158˙121.00

Map

 Project objective

The complexity of autoimmune responses is a barrier to the design of strategies that can selectively purge the immune system of autoreactivity without impairing systemic immunity. Recently, Santamaria et al. have shown that nanoparticles (NPs) coated with type 1 diabetes (T1D)-relevant peptide–MHC (pMHC) complexes can restore normoglycemia in diabetic animals by blunting the diabetogenic autoimmune response without impairing systemic immunity. pMHC class II-NP therapy functions by expanding, in an epitope-specific manner, autoantigen-experienced T-regulatory-1 (TR1) CD4 T-cells that inhibit the recruitment of other autoantigenic specificities by: (1) suppressing autoantigen-loaded antigen-presenting cells in the pancreatic lymph nodes (PLNs); and (2) promoting the differentiation of B-cells into B-regulatory cells. Importantly, they have shown that human T1D-relevant pMHC class II-NPs also promote human TR1 CD4 T-cell formation in NSG mice engrafted with peripheral blood mononuclear cells from recent onset T1D patients.

Here, I propose a multidisciplinary approach to test the following hypotheses: (1) Breg formation is driven by a cognate interaction between TR1 cells and autoreactive B-cells; (2) TR1-derived cytokines play critical roles in TR1-driven Breg conversion in vivo; and (3) the B-cells that are recruited to the PLNs of pMHC-NP-treated humanized NSG mice are enriched for Breg cells. Furthermore, I will work with the enterprise SEPMAG, to design a scalable magnetic separation device for future clinical development of these compounds.

Collectively, NANOBreg will provide new insights into the biology of the TR1-Breg regulatory pathway and will enhance our knowledge on the mechanisms of action of this novel therapeutic approach. In addition, it will address a manufacturing bottleneck by bridging academic research with the manufacturing industry while enhancing my career development in an area of huge potential growth and translational significance.

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The information about "NANOBREG" are provided by the European Opendata Portal: CORDIS opendata.

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