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Blood level of granulysin differs in patients with mild and severe psoriasis

Introduction & Objectives Psoriasis is a chronic inflammatory skin disease mediated by T lymphocytes, while NK and NKT cells are also implicated in its pathogenesis. Granulysin (GNLY) is a pro-apoptotic molecule expressed in the cytoplasmic granules of cytotoxic immune cells. Activated cytotoxic cells such as cytotoxic T lymphocytes (CTLs) and natural killer (NK) cells cause target cell cytolysis by exocytosis of these granules and their contents. Until now, there are few reports regarding the role of granulysin in psoriasis and no data of granulysin blood expression in psoriatic patients. Material & Methods We obtained peripheral blood samples of patients with mild psoriasis, patients with severe psoriasis and healthy controls (10 patients per group). GNLY expression was evaluated in the total lymphocyte population, by direct immunofluorescence staining followed by flow cytometry analyses. Results The objective of our study was to investigate GNLY+ cells in blood lymphocyte population of psoriatic patients and healthy controls. While our previous study showed significantly increased numbers of GNLY+ cells in psoriatic plaques, our present research revealed elevated levels of GNLY+ cells within peripheral blood lymphoctes of psoriatic patients, primely within CD3+CD8+, CD3+CD56+ and CD3- CD56+ cells. The percentage of GNLY+ cells significantly differed between groups of patients with mild and severe psoriasis as well as in group of healthy controls. Conclusions A significant upregulation of GNLY-expressing peripheral blood lymphocytes, especially cytotoxic T cells, NK and NKT cells, has been observed in psoriatic patients in contrast of its level in healthy controls. GNLY-mediated cytotoxicity of peripheral blood lymphocytes considerably differed depending on disease severity. This observation indicates a possible important role of this cytolytic molecule in psoriasis pathogenesis.

Psoriasis, cytotoxic lymphocytes, granulysin, NKT cells

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