Recent studies suggest that activation of Fas serves not only to induce apoptosis, but also to induce the secretion of cytokines and chemokines by a variety of cell types (138) (Figure 2 ). In murine lungs, activation of Fas initiated a pro-found inflammatory response with an early generation of chemokines and subsequent recruitment of neutrophils (130, 132, 139) . This response could be reduced by antagonizing Fas ligand (139) . Triggering of Fas also led to increased concentrations of TNF-α, MIP-1 α, MIP-2, monocyte chemotactic protein (MCP)-1, and IL-6, and compromised the alveolo-capillary barrier (133) . LPSmediated pulmonary inflammation also appears to be regulated through Fas (140) . Mice, genetically altered to express Fas either on myeloid or on nonmyeloid cells in the lung, presented no marked increase of inflammatory mediators following Fas activation (131) , in contrast to non altered mice lungs (130, 132, 139) . With respect to cell types involved, it has been indicated that activation of Fas on monocyte cell lines induced production of MIP-2 (141) . The activation of an inflammatory program by Fas also was shown for peritoneal macrophages (142) , monocytes and macrophages (143) , endothelial cells (144) , and others (145) (146) (147) (148) (149) (150) (151) .