Hofbauer cells (HBCs), are resident macrophages in the villous stroma, that support tissue homeostasis, including debris clearance and tissue remodeling, through high plasticity and responsiveness to the microenvironmental cues. Preeclampsia (PE) is a heterogeneous placental disorder that is characterized by new onset of hypertension during pregnancy, accompanied by at least one additional maternal organ manifestation. It is associated with villous malperfusion, angiogenic imbalance, and inflammatory activation, all of which impair placental function. Based on gestational age at diagnosis, PE is commonly subdivided into early-onset (EO-) and late-onset (LO-) PE. These two subtypes differ in terms of placental pathology, clinical course, and fetal outcome. We hypothesized that the HBCs polarization and effector functions differ between EO- and LO-PE and that these onset-dependent patterns are linked, at least in part, to altered TGF-β superfamily signaling within the villous niche. First, we developed an optimized HBCs isolation and quality control workflow for term placentas to enable reliable profiling. This protocol incorporated strict villous dissection, decidua removal, controlled enzymatic dissociation, Percoll-based enrichment, and flow cytometry following isolation. Quality control was embedded as a core component of the workflow and included viability assessment, purity and identity verification, and exclusion of major contaminants. We demonstrate that PE is associated with onset-dependent changes in HBC polarization and function rather than the development of a single, uniform phenotype. EO-PE exhibited a tissue-remodeling M2 program with a stronger inflammatory component, as evidenced by higher levels of CD86, TLR-4, HLA-DR, IRF5, and NOS2, while maintaining regulatory features, such as ARG1, and increased TGF-β1 secretion. LO-PE exhibited a more phagocytic, CD209-low M2 profile, demonstrating less pronounced inflammatory activation, stronger IRF4 and ARG1 expression, together with increased TGF-β1 secretion and enhanced phagocytosis. Across both subtypes, the core functions of phagocytosis and matrix remodeling remained active which supports maintained plasticity with disease-associated skewing. Next, we reviewed TGF-β superfamily signaling in healthy and PE placentas, examining the trophoblast, endothelial, and immune compartments. Then, we interpreted our findings in relation to these TGF-β patterns. In a healthy pregnancy, TGF-β signaling supports trophoblast differentiation and invasion, angiogenic balance, and the endothelial phenotype. It also promotes immune tolerance by coordinating the effects on Tregs, decidual NK cells, and macrophage polarization. In PE, disruption of TGF-β superfamily signaling is reported at the levels of ligand availability and receptor composition. This is consistent with impaired immune regulation and vascular dysfunction in PE, linking altered TGF-β superfamily signaling to the HBCs phenotypes observed in our study. In conclusion, we developed a reliable HBCs isolation and quality control protocol and applied it to identify distinct, onset-dependent phenotypic and functional HBCs profiles in PE, accompanied by increased TGF-β1 secretion. Integrating these results with the reported disruption of TGF-β superfamily signaling in PE reveals a significant signaling gap. The role of TGF-β superfamily signaling in HBCs remains unclear and further research is needed to investigate ligand bioavailability and receptor balance in relation to macrophage effector programs in onset-stratified PE.