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Cellular mechanisms underlying mast cell - memory T cell interactions in chronic type IV allergic skin inflammation in mice
Giménez Rivera, Vladimir Andrey

HaupttitelCellular mechanisms underlying mast cell - memory T cell interactions in chronic type IV allergic skin inflammation in mice
TitelvarianteZelluläre Mechanismen der Mastzell-Gedächtnis T Zell-Interaktionen in chronischen Typ IV allergischen Hautentzündungen bei Mäusen
AutorGiménez Rivera, Vladimir Andrey
Geburtsort: Bogotá D.C., Colombia
GutachterProf. Dr. Rupert Mutzel
weitere GutachterProf. Dr. Marcus Maurer
Freie SchlagwörterTissue resident memory T cells; Mast cells; chronic contact hypersensitivity
DDC570 Biowissenschaften; Biologie
ZusammenfassungAllergic contact dermatitis (ACD) is a T cell-mediated chronic inflammatory skin condition. ACD is one of the most common occupational diseases worldwide and causes severe quality of life impairment. Mast cells (MCs) are key players in chronic inflammation and involved in the regulation of immune homeostasis and immunosurveillance in various tissues including the skin. As of now, the role of MCs in the chronification of ACD is poorly understood. To address this, we induced chronic contact hypersensitivity (CCHS) to oxazolone (OXA), a contact allergen, in mice as a model for human ACD. Using different murine models, we investigated the role of MCs in CCHS. Mice deficient for MCs or treated with the MC inhibitor cromolyn developed exacerbated CCHS reactions and the reconstitution of MCs in MC-deficient mice prevented this. This exacerbation of inflammation and the protective effects of MCs in CCHS were both restricted to skin sites that had previously been exposed to the allergen, suggesting that MCs control CCHS inflammatory reactions by effects in local skin T cell populations. In support of this, skin areas pre-exposed to allergen showed more tissue resident memory (TRM) CD8β+ T cells in MC-deficient mice. These T cells were found to produce the cytokine interferon gamma (IFNɣ), and this pro-inflammatory cytokine was increased in the inflamed skin during CCHS responses in MC-deficient mice. The reduction of TRM CD8β+ T cells in MC-deficient mice prevented the exacerbation of inflammatory CCHS responses.

In conclusion, these findings demonstrate that MCs protect from exacerbated inflammatory responses in CCHS by controlling the accumulation of local cutaneous TRM CD8β+ T cell populations.
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SeitenzahlV, 132 S.
Fachbereich/EinrichtungFB Biologie, Chemie, Pharmazie
Erscheinungsjahr2015
Dokumententyp/-SammlungenDissertation
Medientyp/FormatText
SpracheEnglisch
Rechte Nutzungsbedingungen
Tag der Disputation10.02.2015
Erstellt am17.03.2015 - 10:11:03
Letzte Änderung17.03.2015 - 10:11:24
 
Statische URLhttp://edocs.fu-berlin.de/diss/receive/FUDISS_thesis_000000098581
URNurn:nbn:de:kobv:188-fudissthesis000000098581-6
Zugriffsstatistik