2026-10-15T08:50:29Z https://data.mendeley.com/oai

oai:data.mendeley.com/7dy5ywnfv3.1 2025-07-07T18:03:10Z

Cao, Yining Trem2 prevents adverse pregnancy outcomes induced by Toxoplasma gondii by promoting PPARγ-mediated P-STAT6 signaling Mendeley Data Decidual macrophages (DMs), required for the maintenance of a successful pregnancy, are vital target cells for Toxoplasma gondii (T. gondii) during adverse pregnancy induced by T. gondii. Trem2 is a functional immune receptor on the surface of DMs, governing cell survival and phagocytosis. Our previous study demonstrated that Trem2 deficiency aggravates T. gondii-induced adverse pregnancy outcomes. However, Trem2-related downstream signaling pathways in T. gondii-induced adverse pregnancy outcomes remains unclear. Here, we demonstrated a significant decrease in PPARγ and phosphorylated-STAT6 (P-STAT6) in mouse placentas following T. gondii infection. By using a Trem2 knockout mouse model, we found that Trem2 deficiency failed to affect the expressions of P-STAT6 and PPARγ in infected mouse placentas, peritoneal macrophages and bone marrow-derived macrophages (BMDMs). Consistently, overexpression of Trem2 in macrophages significantly activated the downstream signaling pathway and partially reversed the inhibitory effects of T. gondii antigens on P-STAT6 and PPARγ, similar to the effect of PPARγ agonists. Altogether, our study identified Trem2 as a key regulator of PPARγ-mediated P-STAT6 signaling pathways in adverse pregnancy outcomes due to T. gondii infection. Our novel findings concerning Trem2 and its downstream PPARγ-mediated P-STAT6 signaling pathways might provide new preventive and therapeutic targets for toxoplasmosis. Immune Response Parasite Immunology Dataset doi:10.17632/7dy5ywnfv3.1 oai:data.mendeley.com/7dy5ywnfv3.1 Creative Commons Attribution 4.0 International http://creativecommons.org/licenses/by/4.0 https://data.mendeley.com/datasets/7dy5ywnfv3 2025-07-07T18:03:10Z