Fig. 3: Effect of regulated cell death on decidual immune cells and stromal cells.
From: The regulated cell death at the maternal-fetal interface: beneficial or detrimental?
A Natural killer (NK) cells can induce apoptosis of smooth muscle cells (SMCs) and endothelial cells (ECs) to promote vascular remodeling. Insufficient autophagy in extravillous trophoblasts (EVTs) or decidual stromal cells (DSCs) can affect the residence and function of NK cells. Galectin-1 secreted by NK cells and macrophages induces apoptosis of CD3+ T cells, while galectin-2 and TSLP inhibit the apoptosis of Treg and γδT cells respectively to maintain immune homeostasis. Ferroptosis facilitates the differentiation of macrophages into the M1 type and autophagy promotes the differentiation into the M2 type. Pyroptosis also affects the differentiation of M2 macrophages. B DSCs can induce the production of Th2 cytokines and promote immune tolerance. Autophagy can promote the decidualization of ESCs to DSCs but ferroptosis plays the opposite role. Lipopolysaccharide (LPS) stimulation can induce the apoptosis of DSCs, increase the secretion of Th1 inflammatory factors, and cause an inflammatory response. Decidual NK (dNK) cells, SGK1, and Tim-3 inhibit LPS-induced apoptosis. Before decidualization, DSCs also secrete pro-apoptotic molecules to induce the apoptosis of undifferentiated DSC. Created with BioRender.com.
