Publications by authors named "V Mraz"
Background: Dysfunction of the skin barrier is regarded as a key event in the initiation and progression of inflammatory skin diseases. In many cases of allergic contact dermatitis (ACD), epidermal-resident memory CD8 T (T) cells play a central role in the immune response to contact allergens. However, if and how allergen-specific CD8 T cells affect the expression of skin barrier molecules is not known.
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- Allergic contact dermatitis (ACD) is a skin condition triggered by the immune system's reaction to haptens, with keratinocytes playing a key role in the inflammatory response and metabolic changes associated with the disease.
- * A study of keratinocytes exposed to contact allergens revealed significant metabolic alterations, indicating an inflammatory response similar to that seen in atopic dermatitis.
- * The findings suggest that ACD involves substantial metabolic re-programming of keratinocytes, marked by changes in pathways related to glucose, fatty acids, and other metabolites upon allergen exposure.
Background: Allergic contact dermatitis (ACD) is an inflammatory disease with a complex pathophysiology in which epidermal-resident memory CD8 T (T ) cells play a key role. The mechanisms involved in the activation of CD8 T cells during allergic flare-up responses are not understood.
Methods: The expression of CD100 and its ligand Plexin B2 on CD8 T cells and keratinocytes before and after allergen exposure was determined by flow cytometry and RT-qPCR.
Background: The junctional adhesion molecule-like protein (JAML) plays important roles in wound healing and activation of epidermal γδ T cells in mice. Whether JAML plays a role in contact hypersensitivity (CHS), the animal model of allergic contact dermatitis (ACD), is not known.
Methods: To examine the role of JAML in CHS, we used various mouse models of CHS in JAML knockout (KO) and wild-type (WT) mice.