• Pattern: MHC class I/II expression is restricted across placental compartments, with extravillous trophoblast displaying MHC I while villous trophoblast lacks it, signaling a curated immune interface. Evidence spans class I/II MHC studies in early to mid-gestation [7], [18], and HLA-DR+ placental cells [1], with broader leukocyte context in early placental beds [3], [11].

• Pattern: Placental mononuclear phagocytes/macrophages are abundant and immunomodulatory, producing cytokines and shaping maternal lymphocyte responses, as shown by isolation, cytokine production (IL-1), and stimulatory interactions with maternal cells [4], [20], [19], [14].

• Pattern: Placental immunoactive products and placental extracts modulate maternal immunity, suppress NK activity and CTL function, and alter alloimmune reactions, illustrating non-specific regulatory signals from placental tissue [13], [17], [16], [8], [5].

• Pattern: Trophoblast-immune cell cross-talk includes maternal T cell stimulation by placental cells, induction of cytotoxic lymphocytes, and antigen-regulated immune interactions, highlighting bidirectional signaling shaping fetal tolerance [9], [15], [14], [18].

• Pattern: Placental barrier and paternal antigen localization underscore selective antigen exposure and trafficking, with paternal antigen localization on trophoblasts and barrier properties limiting cellular passage [6], [12].