OPN-IMMUNOREGULATION

Immune mechanisms of osteopontin-mediated protection in allergic airway disease

 Coordinatore "BIOMEDICAL RESEARCH FOUNDATION, ACADEMY OF ATHENS" 

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 Nazionalità Coordinatore Greece [EL]
 Totale costo 1˙511˙200 €
 EC contributo 1˙511˙200 €
 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-2009-StG
 Funding Scheme ERC-SG
 Anno di inizio 2009
 Periodo (anno-mese-giorno) 2009-12-01   -   2015-11-30

 Partecipanti

# participant  country  role  EC contrib. [€] 
1    "BIOMEDICAL RESEARCH FOUNDATION, ACADEMY OF ATHENS"

 Organization address address: Soranou Efesiou 4
city: ATHENS
postcode: 11527

contact info
Titolo: Dr.
Nome: Vasiliki
Cognome: Panoutsakopoulou
Email: send email
Telefono: +30 210 6597185
Fax: +30210 6597545

EL (ATHENS) hostInstitution 1˙511˙200.00
2    "BIOMEDICAL RESEARCH FOUNDATION, ACADEMY OF ATHENS"

 Organization address address: Soranou Efesiou 4
city: ATHENS
postcode: 11527

contact info
Titolo: Mr.
Nome: Dimitris
Cognome: Raptis
Email: send email
Telefono: +30 210 6597707
Fax: +30 210 6597571

EL (ATHENS) hostInstitution 1˙511˙200.00

Mappa


 Word cloud

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recruitment    mechanisms    airway    pulmonary    regulation    allergen    disease    mice    setting    opn    cells    immunoregulatory    interactions    protection    mediated    responses    dc    allergic    antigenic    inflammation    immune   

 Obiettivo del progetto (Objective)

'In allergic asthma, an important health problem, disease is driven by allergen-specific Th2 immune responses. Differentiation of Th2 cells depends on their early interactions with antigen presenting cells, such as dendritic cells (DCs), and cytokines are crucial for this process. Osteopontin (Opn) was originally identified as an important cytokine for Th1 immunity and autoimmunity. Our group recently demonstrated that Opn is highly expressed in the lungs of asthmatic patients and of mice with Th2-mediated allergic airway inflammation. Our work revealed anti-allergic effects of Opn on airway disease during secondary pulmonary antigenic challenge mediated by regulation of DC subsets. In addition, intranasal administration of recombinant Opn during pulmonary exposure to the allergen protected mice from allergic airway disease suppressing all features of disease, recruitment of Th2 cells and allergen-specific Th2 responses. Our previous experiments, as well as preliminary studies presented in this proposal, point to an important novel immunoregulatory role for Opn in the Th2 setting. However, most aspects of the Opn-mediated immune mechanism of protection remain unclear. With this proposal, we aim at elucidating the immunoregulatory/protective mechanisms of Opn utilizing immunologic, molecular and genomic approaches as well as in vivo mouse models of allergic airway inflammation. We propose to investigate the mechanisms mediating Opn-effects on: (1) DC subsets and Treg cells that confer protection during pulmonary allergen challenge (2) recruitment and function of allergen-specific Th2 (generated during sensitization) as well as of newly-activated Th effector cells and their interactions during pulmonary allergen challenge and (3) antigenic tolerance induction in the Th2 setting. The studies proposed here will provide new insight into the biology of Opn-dependent regulation of DC subsets, Th2 responses and DC-T cell interactions opening new important questions in im'

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