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Am J Physiol Lung Cell Mol Physiol 281: L1248-L1256, 2001;
1040-0605/01 $5.00
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Vol. 281, Issue 5, L1248-L1256, November 2001

Lung fibroblasts inhibit activation-induced death of T cells through PGE2-dependent mechanisms

Timur O. Yarovinsky and Gary W. Hunninghake

Division of Pulmonary, Critical Care, and Occupational Medicine, Department of Internal Medicine, University of Iowa, Iowa City, Iowa 52242

Activation-induced cell death (AICD) is a regulatory mechanism eliminating excess activated T cells, mainly through a Fas/Fas ligand-dependent mechanism. The goal of this study was to determine whether mouse primary lung fibroblasts are capable of modulating AICD. Using T cell hybridoma DO11.10, we found that fibroblasts in coculture rescue T cells from AICD. Fibroblast-conditioned medium (FCM) also inhibited apoptosis of T cells activated with immobilized anti-CD3 antibody. The effects of lung fibroblasts are mediated, in part, by secreted prostaglandin E2 (PGE2) because treatment of fibroblasts with indomethacin decreased antiapoptotic activity of FCM. Addition of exogenous PGE2 to FCM from fibroblast cultures treated with indomethacin restored the inhibitory activity of FCM. Expression of Fas receptor and Fas ligand by anti-CD3-activated DO11.10 cells was not affected by PGE2. However, the same concentrations of PGE2 significantly downregulated activation of caspase-8 and caspase-3. These results demonstrate that lung fibroblasts inhibit the AICD of T cells by secreting PGE2, which downregulates caspase activation and apoptosis.

T lymphocytes; apoptosis; prostaglandins; Fas ligand; caspases


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