Somatostatin immunoreactive cells in lesional psoriatic human skin during peptide t treatment

Abstract

Peptide T has been shown to be an effective treatment in psoriasis. The mechanism through which peptide T works in psoriasis is at present unknown. Furthermore, a clearance of psoriasis has also been registered using the inhibitory peptide somatostatin. These observations all focus on the fact that peptide T, somatostatin, and/or other peptides, might provide a clue to understanding the etiology and pathogenesis of psoriasis. Therefore, the effect of peptide T administration on somatostatin containing cutaneous cell populations was investigated. Ten psoriatic patients were treated with peptide T (D-Ala-peptide T amide; 2 mg/day i.v.) for 28 days. Serial biopsies were obtained from the psoriatic lesions before, once weekly during and 4 weeks after discontinuation of the peptide T treatment. An indirect immunofluorescence procedure was performed using a polyclonal antiserum against somatostatin. Clinically, most of the patients responded successfully to the treatment. Immunohistochemical investigations of the serial biopsies revealed the appearance of extensive changes in the number of dermal somatostatin immunoreactive dendritic cells. We believe that peptide T may stimulate the local synthesis and/or release of somatostatin, or proliferation and/or migration of certain dendritic cell populations in psoriatic lesions during healing. Since the benefits of peptide T treatment of psoriatic patients parallel earlier investigations using somatostatin infusions, it is likely that somatostatin given exogenously or synthesized/released endogenously plays a vital role in inducing the healing process. Because of the very few (so far reported) side-effects of peptide T treatment, as compared to somatostatin (or somatostatin analogue) injections/infusions, there is much hope that peptide T in the future can be used in the medical treatment of the large group of patients suffering from psoriasis.