Perhaps a mechanism by which autoimmunity leads to fluid loss, hypovolemia and POTS/OI. I should note that this article was first brought to my attention by another PR member (whom I would gladly acknowledge but I don't have their permission to do so). I've been away for a while and am just getting back to PR. Thanks to "you know who you are." Cutting edge: Neuronal recognition by CD8 T cells elicits central diabetes insipidus. Scheikl T, Pignolet B, Dalard C, Desbois S, Raison D, Yamazaki M, Saoudi A, Bauer J, Lassmann H, Hardin-Pouzet H, Liblau RS. J Immunol. 2012 May 15;188(10):4731-5. Epub 2012 Apr 13. Abstract An increasing number of neurologic diseases is associated with autoimmunity. The immune effectors contributing to the pathogenesis of such diseases are often unclear. To explore whether self-reactive CD8 T cells could attack CNS neurons in vivo, we generated a mouse model in which the influenza virus hemagglutinin (HA) is expressed specifically in CNS neurons. Transfer of cytotoxic anti-HA CD8 T cells induced an acute but reversible encephalomyelitis in HA-expressing recipient mice. Unexpectedly, diabetes insipidus developed in surviving animals. This robust phenotype was associated with preferential accumulation of cytotoxic CD8 T cells in the hypothalamus, upregulation of MHC class I molecules, and destruction of vasopressin-expressing neurons. IFN-γ production by the pathogenic CD8 T cells was necessary for MHC class I upregulation by hypothalamic neurons and their destruction. This novel mouse model, in combination with related human data, supports the concept that autoreactive CD8 T cells can trigger central diabetes insipidus.