Apoptosis: a target for potentiation of UV-induced IL-1Ra synthesis by IVIg.

IL-1Ra prevents IL-1 induced inflammatory signalling, a mechanism potentially important for several pathological conditions characterized by inflammation. When administered as a drug in the recombinant form, it displays a protective effect towards them. We postulated that this action could also be achieved by pharmacological activation of endogenous IL-1Ra production.

Anti-inflammatory effects of UV-irradiated lymphocytes: induction of IL-1Ra upon phagocytosis by monocyte/macrophages.

One of the mechanisms proposed to explain immunomodulatory actions of ultraviolet light (UV) is production of endogenous anti-inflammatory cytokines. The purpose of the present study is to evaluate how UV light affects the production of IL-10 and IL-1Ra and to provide insight as to the role of phagocytosis of apoptotic lymphocytes in this process. Cytokine production was evaluated in a coculture system consisting in UV-treated lymphocytes in the presence of autologous PBMC.

Increased production of interleukin-10 and interleukin-1 receptor antagonist after extracorporeal photochemotherapy in chronic graft-versus-host disease.

Background: Mechanisms of action of extracorporeal photochemotherapy (ECP) in graft-versus-host disease are incompletely understood. It has been proposed that phagocytosis of apoptotic bodies by monocytes and macrophages induces their activation, a process that increases production of immunosuppressive cytokines. We analyzed apoptosis and cytokine secretion in an autologous coculture system combining peripheral blood lymphocytes (PBL) obtained after ex vivo ECP treatment and nonirradiated peripheral blood mononuclear cells (PBMC).