T-cell mechanisms in atopic dermatitis.

This review provides an overview of recent advances in understanding T-cell inflammation in atopic dermatitis (AD), a common chronic inflammatory skin disease. After recognizing their cognate antigen in the acute phase of the disease, the homing of T cells from the circulation into the skin via cutaneous lymphocyte antigen (CLA) is the prerequisite to skin inflammation and subsequent systemic and local, tissue resident, memory (TRM) formation. Initial observations suggest that antigen presentation occurs in structures such as induced skin-associated lymphoid tissue (iSALT), in addition to lymphatic organs. Aside from environmental antigens, such as aeroallergens, other antigen sources also appear to play a role: humoral and cellular responses to microbial antigens and autoantigens are discussed to drive and shape skin inflammation in AD. In-depth characterization of differentiated, activated Th2 cells in AD shows their ability to recognize different signals from epithelial cells directly. The heterogeneity of patients with antigen sensitizations and T-cell phenotypes is believed to influence therapeutic success. This suggests that a more precise characterization of patient subgroups would enable targeted, individualized therapy.