Phosphatidylserine-dependent ingestion of apoptotic cells promotes TGF-β1 secretion and the resolution of inflammation
J. Clin. Invest. Mai-Lan N. Huynh, et al. 109:41 doi:10.1172/JCI11638 [
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Figure 3In vivo TGF-β1 induction resulted from increased release and de novo synthesis. (
a) The increase in TGF-β1 secretion in thioglycollate-stimulated peritoneum was seen in 30-minute lavages after in vivo instillation of apoptotic Jurkat T cells (ApoJ) and was more pronounced than in the 4-hour lavages. (
b) TPMφ cell-associated TGF-β1 at 1 hour was reduced after in vivo instillation of ApoJ. (
c) Total (secreted + cell-associated) TGF-β1 remained constant. *
P < 0.05,
n = 8, ± SD. (
d) In vitro secretion of TGF-β1 by TPMφ’s was increased after addition of apoptotic Jurkat T cells (ApoJ) compared with media alone (control) at 4 and 18 hours (*
P < 0.05). TGF-β1 secretion in both control and ApoJ-treated macrophages was markedly inhibited by preincubation with cycloheximide (5 μg/ml) for 1 hour. **
P < 0.001,
n ≥ 13, ± SD.
