Cell-mediated immune response in psoriasis and psoriatic arthritis

It has been previously described an impairment of cell-mediated immune response in psoriasis. In the present paper we have evaluated lymphocyte surface markers, non specific immunity, lymphokine secretion and antibody synthesis in a group of patients with psoriasis (PS) and with anti-inflammatory drug treated or gold-treated psoriatic arthritis (PsA). No significant differences are found in terms of T lymphocyte subpopulation frequency, even if a lower CD8+/CD4+ ratio was observed in all patients. In spite of an increased percentage of B lymphocytes, B cell polyclonal response is significantly decreased in the presence of either T cell-independent or T cell-dependent polyclonal activator. Further studies provide additional supports to these findings, since all psoriatic patients exhibit a deficit of T helper function in an antibody-specific induction system. Gold therapy in PsA led to a partial recovery of T helper function, without affecting the immunoglobulin reduced synthesis. With particular reference to non-specific activities mediated by monocytes and polymorphs (PMN), PMN chemotaxis, phagocytosis and killing and monocyte-mediated phagocytosis are reduced, except for monocyte phagocytosis in anti-inflammatory treated PsA or PMN chemotaxis in gold-treated PsA. Finally, lymphokine release is significantly decreased in all patients. In conclusion, our data provide further evidence for the impairment of immune response in psoriasis and PsA, which may in turn play a key role in the pathogenesis of psoriasis.