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. Author manuscript; available in PMC: 2014 Apr 1.
Published in final edited form as: J Immunol. 2013 Mar 1;190(7):3639–3647. doi: 10.4049/jimmunol.1203488

Figure 7. Schematic representation of the poly(I:C)-induced events in WT and IL-10−/− mice.

Figure 7

The model recapitulates the pathways leading to uterine NK or T cell-mediated cytotoxicity and fetal resorption in WT and IL-10−/− mice, respectively. Rae-1 positive macrophages or trophoblasts can interact with NKG2D+ NK cells and induce TNF-α production and trophoblast cell death in response to poly(I:C). On the other hand, uterine T cells can be activated by poly(I:C) in the absence of IL-10 to produce TNF-α and to cause fetal demise.