Breakdown of this HF immune privilege is thought to be essential for the onset of AA (31), likely occurring when the balance of signaling pathways upholding this immune privilege is overwhelmed by those leading to collapse, including interferon (IFN)-γ–induced upregulation of MHC classes I and II antigen-presenting molecules, loss of local TGF-β–dependent immunosuppression, increased MICA expression, decreased MIF expression, and mast cell degranulation (43). Here, TGFB1 is linked to hydrops fetalis.