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BEAT SIGNED

regulation of B-cell Epitope migration and Autoimmunity by T follicular helper cells

Total Cost €

EC-Contrib. €

Partnership

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BEAT project word cloud

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

combination epitope gc play artemis dependent nature behavior prominent clone outgoing deposition damage laboratory migration immunity reactive human chimera pathogenic reaction tolerance altered murine initial involvement excessive strains antigens autoantibody independent helper broken prior expansion microscopy drift photon multiple cell bone trigger dependence self favor autoreactive visualize detection organ marrow therapeutic onset centers few follicular analyze germinal cells function disease single autoimmune intravital once drives autoreactivity natural utilizing tfh reflects spreading followed wt autoantibodies mixed transition kidney carroll activation spontaneous appear clinical model preliminary reactivity differentiation maturation utilize interactions linked dynamic

Project "BEAT" data sheet

The following table provides information about the project.

Coordinator	UNIVERSITAIR MEDISCH CENTRUM UTRECHT Organization address address: HEIDELBERGLAAN 100 city: UTRECHT postcode: 3584 CX website: www.umcutrecht.nl 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	Netherlands [NL]
Total cost	260˙929 €
EC max contribution	260˙929 € (100%)
Programme	1. H2020-EU.1.3.2. (Nurturing excellence by means of cross-border and cross-sector mobility)
Code Call	H2020-MSCA-IF-2017
Funding Scheme	MSCA-IF-GF
Starting year	2018
Duration (year-month-day)	from 2018-07-01 to 2021-06-30

Partnership

Take a look of project's partnership.

#	participants	country	role	EC contrib. [€]
1	UNIVERSITAIR MEDISCH CENTRUM UTRECHT UNIVERSITAIR MEDISCH CENTRUM UTRECHT Organization address address: HEIDELBERGLAAN 100 city: UTRECHT postcode: 3584 CX website: www.umcutrecht.nl contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	NL (UTRECHT)	coordinator	260˙929.00
2	CHILDREN'S HOSPITAL CORPORATION CHILDREN'S HOSPITAL CORPORATION Organization address address: LONGWOOD AVENUE 300 city: BOSTON postcode: 2115 website: http://www.childrenshospital.org/ contact info title: n.a. name: n.a. surname: n.a. function: n.a. email: n.a. telephone: n.a. fax: n.a.	US (BOSTON)	partner	0.00

Map

Project objective

The detection of autoantibodies typically appear a few years prior to clinical autoimmune disease and their reactivity can drift at or after disease onset. The laboratory of M.C. Carroll (outgoing institute) has developed a murine model (ARTEMIS; Autoreactive B-cell driven T-dependent Epitope Migration towards Immunity to Self) where the presence of a single autoreactive B cell clone drives activation, expansion and differentiation of other autoreactive B-cells in spontaneous germinal centers (GC) followed by autoantibody deposition in the kidney. These autoreactive B-cells target multiple other self-antigens (also known as epitope spreading) and are independent of the initial trigger once tolerance is broken. Follicular T helper (Tfh) cells play a prominent role in the selection of B-cells in the GC and have been linked to excessive GC formation, high-level production of pathogenic autoantibodies and end-organ damage in murine and human autoimmune disease. With this project I will address the role of Tfh cells in the maturation process of the self-reactive B-cell response and epitope spreading as observed in human autoimmune disease. Preliminary results show dependence of T cells, the extent and nature of T-cell involvement is however not yet addressed. I will utilize the mixed bone-marrow chimera model (ARTEMIS) in combination with selected strains altered in important factors for Tfh function and differentiation. As the GC reaction is a highly dynamic process we will visualize this utilizing multi-photon intravital microscopy and analyze important interactions of Tfh cells in the developing autoreactive GC. The development of autoreactivity from WT B-cells in the ARTEMIS model better reflects natural autoreactive GC behavior and human autoimmune disease and could therefore favor the transition of potential therapeutic targets from murine to human disease.

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