Differential responses of rat trophoblast cells and embryonic fibroblasts to cytokines that regulate proliferation and class I MHC antigen expression
Hunt, J.S.; Atherton, R.A.; Pace, J.L.
Journal of Immunology 145(1): 184-189
1990
ISSN/ISBN: 0022-1767 PMID: 2113554 Document Number: 352817
TNF-.alpha. and type I IFN (IFN-.alpha./.beta.) are present in the uteroplacental unit during the course of normal gestation. IFN-.gamma. is likely to be present during infections. To identify potential effects on two types of blastocyst-derived cells, TNF-.alpha., IFN-.alpha./.beta., and IFN-.gamma. were tested for the ability to modulate proliferation and the expression of class I MHC Ag by rat trophoblast cells and embryonic fibroblasts. The three cytokines had opposte influences on cellular proliferation by the two types of cells. Growth of the trophoblast cells was inhibited by TNF-.alpha., IFN-.alpha./.beta., and IFN-.gamma., whereas both TNF-.alpha. and IFN-.alpha./.beta. enhanced fibroblast proliferation. The two endogenous cytokines had different effects on class I Ag expression by trophoblast cells and fibroblasts: TNF-.alpha. failed to induce trophoblast cell class I Ag and IFN-.alpha./.beta. was a poor inducer whereas fibroblast Ag were induced by both cytokines. Moreover, combination of TNF-.alpha. and IFN did not increase trophoblast cell class I Ag whereas the same combinations synergized to induce class I Ag expression by fibroblasts. In contrast, IFN-.gamma. was a highly efficient inducer on both types of cells. The results suggest that 1) cytokines in the uteroplacental unit may orchestrate some of the events associated with placental and embryonic development by exerting differential effects on two embryologically distinct types of cells and that 2) infections may disrupt normal events.