Sixty-two skin samples from patients with a variety of benign disorders (20 cases of psoriasis, 14 cases of chronic dermatitis, 11 seborrhoeic ]i:eratoses, 11 cases of lichen planus), and seven normal skin samples, were stained immunohistochemically with a polyclonal antibody (CM-1) to p 5 3, and a monoclonal antibody to Ki67. using the avidin-biotin complex method. p53-positive keratinocytes could be found in most of these lesions. The percentage of p53-positive cells was, however, far lower than usually seen in p53-positive malignant tumours. No p53 reactivity was observed in the normal skin samples. Variable Ki67 reactivity was observed in all skin samples. Overall, the number of Ki67positive cells was higher in skin samples in which the proportion of p53-positive cells was high (> 05% oftotal epidermal cell population) (P -0 004). This also applied separately to psoriatic and non-psoriatic lesions (P -0 028 and P = 0 033, respectively). In cases with > lO^/i of Ki67-positive cells, there were significantly more mitoses (P < OOOl), This association applied to both psoriasis and the other lesions studied (P -0 024 and P< OOOl, respectively). The results show that immunohistochemically detectable accumulation of p53 is a frequent finding in non-neoplastic skin lesions. As p53 positivity was associated with the proliferation marker Ki67. the accumulation of p53 is possibly a response to an increased proliferation rate of the keratinocytes in these skin diseases, or alternatively it may be associated with apoptosis.
Signal transduction by the T-cell and B-cell antigen receptors and receptors for immunoglobulin Fc regions depends highly on the cytoplasmic immunoreceptor tyrosine-based activation motif (ITAM). After binding of the ligand, phosphorylation of the two conserved tyrosines of ITAM creates binding sites for downstream signalling molecules and thus enables the initiation of signalling events. Here, we report that the recently found apoptosis receptor, WSL-1/DR3/APO-3/LARD/TRAMP also contains this motif. This may imply that the apoptosis receptor uses ways similar to immunoreceptors in relaying the induction/suppression of the apoptotic signal.
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