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IL‐10 induces apoptosis in human monocytes involving the CD95 receptor/ligand pathway

The cytokine IL‐10 exerts potent immunosuppressive and anti‐inflammatory effects, although the mechanisms of this action remain largely unknown. In the present study, we investigated the effects of IL‐10 in human peripheral blood monocytes. We were able to demonstrate that IL‐10 dose‐ and time‐dependently triggers apoptosis in these cells as detected by annexin‐V staining, the nick end labeling (TUNEL) procedure, electron microscopy and analysis of DNA laddering. IL‐10‐induced apoptosis required the activation of proteases of the caspase family, since a peptide caspase inhibitor attenuated cell death and, in addition, the proteolytic activation of caspase‐8 was observed. Since caspase‐8 has been implicated as a regulator of apoptosis mediated by death receptors, we investigated a potential involvement of the CD95 receptor/ligand system. Indeed, treatment of monocytes with IL‐10 induced a dose‐dependent up‐regulation of CD95 receptor and ligand expression on the monocyte surface. Furthermore, a CD95 ligand‐neutralizing antibody significantly inhibited IL‐10‐induced apoptosis. In summary, our data show that IL‐10 triggers monocyte apoptosis involving the CD95 system via an autocrine or paracrine process. Therefore, at least part of the anti‐inflammatory properties of IL‐10 may involve induction of apoptosis in monocytes.