However, apoptosis is genuinely designed to actually prevent inflammatory reactions to cell death, and ingestion of apoptotic cells by macrophages induces the expression of anti-inflammatory cytokines such as TGF-β and IL-10, both promoting the expression of Tregs, suppressing an autoimmune response during apoptosis [160] . While apoptosis per se is a non-inflammatory process, it can lead to abnormal antigen presentation, especially of previously sequestered antigens. Evidence for a role in the development of autoimmune disease, however, is limited and particularly in organ-specific autoimmune diseases [178] . Whether apoptosis-related mechanisms lead to PBC is unclear [179] , but cholangiocytes in PBC may undergo increased cell turnover, e.g., due to metabolic stress, resulting in an inadequate immune response [179] . Strikingly, BECs in patients with PBC seem to be under significantly increased apoptotic stress compared to healthy controls or patients with other causes of inflammatory reactions in the liver, such as chronic viral hepatitis or PSC [180] [181] [182] . However, it is yet to be elucidated whether this effect is really a cause of autoimmunity in PBC or rather the consequence of increased inflammation.