LAUSR

In psoriasis, regulatory T cells (Tregs) can modulate the function of effector Th cells and mast cells (MCs) (1, 2). Defined by their expression of CD4, CD25, and the transcription factor forkhead box P3 (FoxP3), Tregs are central in protecting an individual from autoimmune diseases. FoxP3 is a nuclear protein that is considered to be a master regulator in the development and function of Tregs (3, 4). There have been few studies on Tregs in psoriasis; however, it is known that the function of Tregs is impaired in psoriasis, in the lesional skin and in the peripheral blood, with respect to their ability to suppress effector T cells. Treatment of psoriasis may increase the numbers and activity of Tregs (5–7). MC activation is one of the earliest morphological changes in the developing psoriatic lesion (2), but it is unknown to what extent pro-inflammatory MC cytokines are involved in the development of psoriatic lesions. The interaction between Tregs and MCs has been shown to be essential for immunosuppression in a variety of experimental models, such as hepatocarcinoma, colorectal carcinoma, and skin allografts (8–10). The purpose of this study was therefore to investigate Tregs and their interaction with MCs in the early developing lesion in psoriasis. To this end, the tape-stripping technique was used to induce the Köbner reaction, and a series of skin biopsies was obtained at 0 days, 2 h, 1 day, 3 days and 7 days (11, 12). Patients who did not develop the Köbner reaction were the focus of this study, because we hypothesized that suppressive factors prevent the development of lesions compared with patients with positive Köbner reactions. These biopsies were analysed for expression of CD25/IL-2Rα and FoxP3 and for apparent morphological contacts (AMCs) between tryptase-positive MCs and FoxP3+ cells by immunohistochemistry and double-staining. FoxP3 has been described as the marker of Tregs, but it may also be expressed by other cell types. This aspect must be remembered when interpreting the results.