T Cells Induce Prolonged Downregulation of Barrier Molecules in a Mouse Model of Allergic Contact Dermatitis.

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.

CD100 boosts the inflammatory response in the challenge phase of allergic contact dermatitis in mice.

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.

The junctional adhesion molecule-like protein (JAML) is important for the inflammatory response during contact hypersensitivity.

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.

CD4 T cells inhibit the generation of CD8 epidermal-resident memory T cells directed against clinically relevant contact allergens.

Background: CD8 epidermal-resident memory T (T ) cells play central roles in local flare-up responses to experimental contact allergens by inducing massive influx of neutrophils to the epidermis upon allergen challenge. Whether similar immunopathogenic mechanisms are involved in the responses to clinically relevant contact allergens is unknown.

Methods: The immune response to cinnamal, ρ-phenylenediamine (PPD) and methylisothiazolinone (MI) was studied in a well-established mouse model for allergic contact dermatitis that includes formation of T cells by ELISA, flow cytometry, fluorescence microscopy analyses and cell depletion protocols.

CD8 tissue-resident memory T cells recruit neutrophils that are essential for flare-ups in contact dermatitis.

Background: Allergic contact dermatitis (ACD) is classically described as a delayed-type hypersensitivity reaction. However, patients often experience flare-ups characterized by itching erythema, edema, and often vesicles occurring within hours after re-exposure of previously sensitized skin to the specific contact allergen. Recent studies have indicated that skin-resident memory T (T ) cells play a central role in ACD.

Epidermal T cell subsets-Effect of age and antigen exposure in humans and mice.

Background: Epidermal T cells play a central role in immune surveillance and in inflammatory skin diseases. Major differences in the epidermal T cell composition are found between adult humans and antigen-inexperienced laboratory mice. Whether this is due to inborn species differences, to different environmental exposures, or a combination of the two is a matter of debate.

γδ T cells and inflammatory skin diseases.

Approximately 25% of the population suffers from skin diseases. The most common forms of skin diseases are the inflammatory skin diseases such as allergic contact dermatitis, psoriasis, and atopic dermatitis. These diseases are described as T cell-mediated diseases induced by either allergens or autoantigens.

Pathogenic CD8 Epidermis-Resident Memory T Cells Displace Dendritic Epidermal T Cells in Allergic Dermatitis.

The skin is our interface with the outside world, and consequently it is exposed to a wide range of microbes and allergens. Recent studies have indicated that allergen-specific skin-resident memory T (T) cells play a role in allergic contact dermatitis (ACD). However, the composition and dynamics of the epidermal T-cell subsets during ACD are not known.

Mice with epidermal filaggrin deficiency show increased immune reactivity to nickel.

Background: Nickel allergy and dermatitis have been associated with filaggrin gene mutations in epidemiological studies, but the mechanisms mediating these associations are unknown.

Objectives: To investigate whether filaggrin-deficient flaky tail (ft/ft) mice show increased immune reactivity to nickel and elucidate the mechanisms mediating this.

Methods: The immune responses to nickel, 2,4-dinitrofluorobenzene (DNFB), cinnamal and p-phenylenediamine were assessed in ft/ft and wild-type (WT) mice.

Increased Production of IL-17A-Producing γδ T Cells in the Thymus of Filaggrin-Deficient Mice.

Mutations in the filaggrin gene () are associated with increased systemic levels of Th17 cells and increased IL-17A production following antigen exposure in both humans and mice. In addition to Th17 cells, γδ T cells can produce IL-17A. The differentiation of γδ T cells to either IFNγ or IL-17A-producing (γδT17) cells is mainly determined in the thymus.