Objective
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.
Fields of science (EuroSciVoc)
CORDIS classifies projects with EuroSciVoc, a multilingual taxonomy of fields of science, through a semi-automatic process based on NLP techniques.
CORDIS classifies projects with EuroSciVoc, a multilingual taxonomy of fields of science, through a semi-automatic process based on NLP techniques.
- medical and health scienceshealth sciencesinflammatory diseases
- medical and health scienceshealth sciencesinfectious diseases
- medical and health sciencesbasic medicineimmunology
- medical and health sciencesbasic medicinephysiologyhomeostasis
- medical and health sciencesclinical medicinenephrologykidney diseases
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Programme(s)
Funding Scheme
MSCA-IF-EF-ST - Standard EFCoordinator
1067-001 LISBOA
Portugal