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Anna Russano

Researcher at University of Perugia

Publications -  15
Citations -  594

Anna Russano is an academic researcher from University of Perugia. The author has contributed to research in topics: T cell & Antigen. The author has an hindex of 10, co-authored 14 publications receiving 562 citations.

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Human CD1-restricted T cell recognition of lipids from pollens

TL;DR: Evidence is provided that pollen lipids may be recognized as antigens by human T cells through a CD1-dependent pathway and allergic, but not normal subjects, displayed circulating specific IgE and cutaneous weal and flare reactions to phospholipids.
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Recognition of pollen-derived phosphatidyl-ethanolamine by human CD1d-restricted γδ T cells

TL;DR: CD1d-restricted γδ T cells specific for phospholipids can represent a key mucosal regulatory subset for the control of early host reactivity against tree pollens and expand the possibilities in diagnostic and therapeutic interventions.
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CD1-Restricted Recognition of Exogenous and Self-Lipid Antigens by Duodenal γδ + T Lymphocytes

TL;DR: A substantial percentage of TCRγδ+ but few TCRαβ+ from human duodenal mucosa recognize exogenous phospholipids in a CD1-restricted fashion, which could contribute to mucosal homeostasis, but could also favor the emergence of inflammatory or allergic intestinal diseases.
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Biological effects of montelukast, a cysteinyl‐leukotriene receptor‐antagonist, on T lymphocytes

TL;DR: Montelukast has anti‐inflammatory activity in the treatment of allergic diseases but whether this effect is due only to blocking leukotrienes or also owing to inhibiting proliferation and survival of inflammatory cells, is actually unknown.
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Defective Expression of Fas Messenger RNA and Fas Receptor on Pulmonary T Cells from Patients with Asthma

TL;DR: T cells from the lungs of untreated persons with asthma express Fas receptor are investigated, showing the persistence of allergen-specific T cells at the mucosal surfaces of atopic persons results from local defective surface expression of Fas receptor and subsequent impairment in active, allergenic-driven cell death.