It's not ineptitude that keeps immune cells in human embryonic skin from reacting to motherly tissue. According to Schuster et al. on page 169, the cells are suppressed from the get-go.
Theories on how developing embryos prepare their immune system for adult life but keep it in check before birth have mainly been generated from studies in mice. Some hypotheses predict that embryonic immune cells are too immature or too few in number to mount an adequate response. Here, Schuster et al. study dendritic cell (DC) ontogeny in the skin of human embryos and find that the cells are functional within the first trimester but are kept in check by a suppressive environment.
DCs from embryonic skin up-regulated costimulatory molecules and stimulated T cells, proving their functional capability. But this potential may be dampened in situ by the high levels of the immunosuppressive cytokine IL-10 that the authors found in embryonic tissues.
Comparing precursors of skin-specialized Langerhans cells (LCs) from embryos of various ages revealed evidence of a stepwise progression of epidermal LC development. By the ninth week of gestation, DCs had appeared in the epidermis—likely drawn in by the high levels of chemokines expressed there and in the dermis—and appeared to be proliferating. At that time, some of the cells expressed CD1c, and only later acquired langerin and CD1a, identifying them as mature Langerhans cells.
Experimental evidence revealing the mechanisms behind DC migration, proliferation, and maturation in developing skin may be a long time coming, says Schuster, largely because of the ethical constraints involved in embryonic research.
