Читать книгу Autoimmune Liver Disease - Группа авторов - Страница 78

Autoimmunity begins with loss of tolerance to a specific autoantigen, but later expands to include reactions to additional autoantigens, a phenomenon called epitope spreading [1]. By extending the autoreactive T‐cell and B‐cell repertoire mediating autoimmune disease, epitope spreading greatly reduces the prospect that host immunoregulatory mechanisms can resume control. The causes of epitope spreading are poorly defined but may involve failure of normal anti‐inflammatory mechanisms of apoptosis or other forms of efferocytosis to prevent presentation of autoantigens. The hypothesis that apoptosis is involved in epitope spreading is attractive because apoptotic blebs do not contain random samples of intracellular constituents, but instead contain high concentrations of known autoantigens.