Evaluation of the profile of the immune cell infiltrate in lichen planus, discoid lupus erythematosus, and chronic dermatitis.

AIMS: The term 'interface dermatitis' refers to those dermatoses in which an inflammatory process involves the dermoepidermal junction, with injury and even necrosis of the basal cell keratinocytes. Interface dermatitis can be characterised further as being either vacuolar or lichenoid changes. Immune cell infiltrate is a constant feature in interface dermatitis. In this study, we hypothesised that 'the profile of the immune cell infiltrate varies between lichenoid and vacuolar interface dermatitis'. This investigation tries to test this hypothesis and to characterise immune cells in interface dermatitis.

METHODS: Thirty-one interface dermatitis lesions (interface dermatitis group: 19 cases of lichen planus, LP; and 12 cases of discoid lupus erythematosus, DLE) and 20 specimens of normal skin (control group) were examined using immunoperoxidase staining methods. Antibodies targeting histiocytes/dendritic cells (CD68+), T cells (CD3+), B cells (CD20+), T cells with either cytotoxic potential (TIA-1+) or cytotoxic activity (Granzyme-B+) were used to decorate the immune cells. In addition, 16 cases of chronic dermatitis [lichen simplex chronicus (LSC), non-interface dermatitis group] were included to substantiate findings in the interface dermatitis group. The results were scored as mean values of positively stained immune cells.

RESULTS: The numbers of immune cells were significantly high (p < 0.05) in the lesional skin (LP, DLE and LSC) compared with normal skin. The most prevalent cell populations were CD3+ T lymphocytes followed by CD68+ cells. Most of the CD3+ cells were resting (TIA-1+, cytotoxic potential) rather than active T cells (Granzyme-B+, active cytotoxicity). Numeric variations were seen between interface and chronic dermatitis groups with significant increase of the density of immune cells in the interface dermatitis (p < 0.05). We found some variations in the composition and distribution of immune cell infiltrate between LP (lichenoid change) and DLE (vacuolar changes). The mean counts of CD3+ cells were high in LP compared with DLE (p < 0.05). Alternatively, the density of CD20+ cells was high in DLE compared with LP (p < 0.05). High density of CD3+ (perivascular location and dermoepidermal junction, p < 0.05) positively stained cells was found in LP compared with DLE. In contrast, high density of CD20+ (perivascular location and dermoepidermal junction, p < 0.05), TIA-1+ and Granzyme-B+ (perivascular location and dermoepidermal junction, p > 0.05) positively stained cells was observed in DLE compared with LP.

CONCLUSIONS: Here we report some variations in the profile (density and positioning) of the immune cell infiltrate between LP and DLE. These variations include high density of CD68+ cells and CD3+ T lymphocytes in LP and DLE; and the numeric dominance of CD20+ B-lymphocytes in DLE compared with LP. Also, some differences in the density of TIA-1+ and Granzyme-B+ cytotoxic T cells between LP and DLE were observed. Our findings suggest a possible link between the type of these cells and the development of interface dermatitis lesions. The possible ramifications of these findings are open for further investigations.