Critical role of rabphilin-3A in the pathophysiology of experimental lymphocytic neurohypophysitis.

摘要: Autoimmune hypophysitis (AH) is thought to be an autoimmune disease characterized by lymphocytic infiltration of the pituitary gland. Among AH pathologies, infundibulo-neurohypophysitis (LINH) involves neurohypophysis and/or hypothalamic infundibulum, causing central diabetes insipidus resulting from insufficiency arginine vasopressin secretion. The pathophysiological and pathogenetic mechanisms underlying LINH are largely unknown. Clinically, differentiating other diseases accompanied mass lesions, including tumours, has often been difficult, because similar clinical manifestations. We recently reported that rabphilin-3A autoantigen anti-rabphilin-3A antibodies constitute a possible diagnostic marker for LINH. However, involvement in pathogenesis remains elucidated. This study was undertaken explore role neurohypophysitis investigate mechanism. found immunization mice with led neurohypophysitis. Lymphocytic observed supraoptic nucleus 1 month after first immunization. Mice immunized showed increase volume urine hypotonic as compared control mice. Administration cocktail monoclonal did not induce abatacept, which chimeric protein suppresses T-cell activation, decreased number T cells specific peripheral blood mononuclear (PBMCs). It ameliorated CD3+ had rabphilin-3A. Additionally, there linear association between PBMCs infiltrating neurohypophysis. In conclusion, we suggest pathogenic antigen, involved Copyright © 2018 Pathological Society Great Britain Ireland. Published John Wiley & Sons, Ltd.