REGDAM | REGULATORY T CELLS AND TISSUE DAMAGE CONTROL

Summary
Regulatory T cells (TREG) are critical players in the control of innate and adaptive immune responses while impacting as well on the functional output of parenchyma tissues. This later effect is exerted by tissue-resident TREG, via an ill-defined mechanism that modulates tissue damage control, that is, a protective response of parenchyma tissues that limits cellular dysfunction and/or damage imposed by inflammation and immunity. The central hypothesis to be tested under this proposal is that tissue-resident TREG modulate tissue damage control via a number of adaptive responses to cellular stress, which preserve the functional outputs of parenchyma tissues. Failure of tissue-resident TREG to modulate adaptive responses to oxidative and hypoxic stress should exacerbate the deleterious effects imposed by these forms of stress on parenchyma cells and as such promote the pathogenesis of immune mediated inflammatory diseases. Under this Marie-Curie fellowship we will address mechanistically how TREG receive signals from tissues exposed to oxidative and hypoxic stress and migrate to those tissues to modulate oxidative and hypoxic stress responses as to dampen tissue damage.
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More information & hyperlinks
Web resources: https://cordis.europa.eu/project/id/707998
Start date: 01-04-2017
End date: 31-03-2019
Total budget - Public funding: 148 635,60 Euro - 148 635,00 Euro
Cordis data

Original description

Regulatory T cells (TREG) are critical players in the control of innate and adaptive immune responses while impacting as well on the functional output of parenchyma tissues. This later effect is exerted by tissue-resident TREG, via an ill-defined mechanism that modulates tissue damage control, that is, a protective response of parenchyma tissues that limits cellular dysfunction and/or damage imposed by inflammation and immunity. The central hypothesis to be tested under this proposal is that tissue-resident TREG modulate tissue damage control via a number of adaptive responses to cellular stress, which preserve the functional outputs of parenchyma tissues. Failure of tissue-resident TREG to modulate adaptive responses to oxidative and hypoxic stress should exacerbate the deleterious effects imposed by these forms of stress on parenchyma cells and as such promote the pathogenesis of immune mediated inflammatory diseases. Under this Marie-Curie fellowship we will address mechanistically how TREG receive signals from tissues exposed to oxidative and hypoxic stress and migrate to those tissues to modulate oxidative and hypoxic stress responses as to dampen tissue damage.

Status

CLOSED

Call topic

MSCA-IF-2015-EF

Update Date

28-04-2024
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Horizon 2020
H2020-EU.1. EXCELLENT SCIENCE
H2020-EU.1.3. EXCELLENT SCIENCE - Marie Skłodowska-Curie Actions (MSCA)
H2020-EU.1.3.2. Nurturing excellence by means of cross-border and cross-sector mobility
H2020-MSCA-IF-2015
MSCA-IF-2015-EF Marie Skłodowska-Curie Individual Fellowships (IF-EF)