Background: IL-10 production by LPS or anti-CD3 stimulated newborn BMLs is greatly reduced, and TNF-α stimulates IL-10 production by adult BMLs. Since TNF-α production may be developmentally delay, we tested whether exogenous TNF-α increases IL-10 production by newborn cells. Methods: Adult and newborn BMLs were cultured with LPS and/or human recombinant TNF-α for 24h. Cell viability was tested by trypan-blue exclusion. IL-10 in supernatants from the cultures was quantified by ELISA. Results: Production of IL-10 by unstimulated adult (185 pg/ml) or newborn (121 pg/ml) BMLs was low. Mean ± SD production of IL-10 increased in adult BMLs stimulated by LPS (49111 3041 pg/ml), TNF-α alone (1520 ± 1395 pg/ml), or with LPS and TNF-α (5380 ± 3190 pg/ml), but not in newborn BMLs (LPS, 1306 ± 1216 pg/ml, p < 0.01; TNF-±, 211 ± 207 pg/ml, p < 0.01; both agents, 1225 ± 971 pg/ml, p < 0.01). Conclusions: Little IL-10 is produced by newborn BMLs in response to exogenous TNF-±. Thus, these experiments suggest that the developmental delay in IL-10 production by human newborn BMLs is not due to the paucity of intrinsic production of TNF-±, but to other mechanisms.
|Original language||English (US)|
|Journal||Journal of Investigative Medicine|
|State||Published - 1996|
ASJC Scopus subject areas
- Biochemistry, Genetics and Molecular Biology(all)