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Emira Ayroldi

Researcher at University of Perugia

Publications -  76
Citations -  4335

Emira Ayroldi is an academic researcher from University of Perugia. The author has contributed to research in topics: Apoptosis & T cell. The author has an hindex of 29, co-authored 73 publications receiving 4064 citations. Previous affiliations of Emira Ayroldi include University of Messina.

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A new dexamethasone-induced gene of the leucine zipper family protects T lymphocytes from TCR/CD3-activated cell death.

TL;DR: GILZ expression selectively protects T cells from apoptosis induced by treatment with anti-CD3 monoclonal antibody but not by treatment of other apoptotic stimuli, and correlates with inhibition of Fas and Fas ligand expression.
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GITR, a member of the TNF receptor superfamily, is costimulatory to mouse T lymphocyte subpopulations

TL;DR: The results show that the proliferation response of CD8+ and CD4+ peripheral T cell subpopulations was potentiated when a GITR costimulus was added to an anti‐CD3 stimulus, suggesting a novel function for G ITR as costimulatory molecule of T cell subsets.
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Reverse signaling through GITR ligand enables dexamethasone to activate IDO in allergy.

TL;DR: It is shown that reverse signaling through GITRL after engagement by soluble GITR initiates the immunoregulatory pathway of tryptophan catabolism in mouse plasmacytoid dendritic cells, by means of noncanonical NF-κB–dependent induction of indoleamine 2,3-dioxygenase (IDO).
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Modulation of T-cell activation by the glucocorticoid-induced leucine zipper factor via inhibition of nuclear factor κB

TL;DR: A new molecular mechanism involved in the dexamethasone-induced regulation of NF-kappaB activity and T-cell activation is identified and is identified as GILZ-mediated modulation of TCR-induced responses.
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Glucocorticoid-induced leucine zipper (GILZ): a new important mediator of glucocorticoid action

TL;DR: The finding that GILZ silencing abrogates the antiproliferative activity of dexamethasone and reduces GC inhibition of cytokine‐induced COX‐2 expression clearly gained GILz a distinguished reputation within the critical mediators of GC effects.