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.

Induced Human Regulatory T Cells Express the Glucagon-like Peptide-1 Receptor.

The glucagon-like peptide-1 receptor (GLP-1R) plays a key role in metabolism and is an important therapeutic target in diabetes and obesity. Recent studies in experimental animals have shown that certain subsets of T cells express functional GLP-1R, indicating an immune regulatory role of GLP-1. In contrast, less is known about the expression and function of the GLP-1R in human T cells.

The role of interleukin-1β in the immune response to contact allergens.

Interleukin-1β (IL-1β) is an important pro-inflammatory cytokine that has an effect on almost every cell lineage in the body. By blocking IL-1β and investigating the IL-1β signaling pathway, several studies have demonstrated a central role of IL-1β in the response to contact allergens. This review summarizes the current literature regarding the basic immunological mechanisms mediated by IL-1β in the different phases of allergic contact dermatitis (ACD) and highlights potential IL-1β-targeted treatment options, which in the future may be relevant in the treatment of patients with ACD.

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.

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.

Dendritic Epidermal T Cells in Allergic Contact Dermatitis.

Allergic contact dermatitis (ACD) is a common inflammatory skin disease with a prevalence of approximately 20% in the European population. ACD is caused by contact allergens that are reactive chemicals able to modify non-immunogenic self-proteins to become immunogenic proteins. The most frequent contact allergens are metals, fragrances, and preservatives.

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.