Target it All Right But Do Not Forget the Torchbearer
Ischemia is frequent in clinical practice and extends beyond trauma to solid organ transplantation, and vasculitis to mention a few. Ischemia and a number of additional stressors condition cells and tissues to express new antigens. Previously, it was recognized that apoptosis enables the formation of blebs on the surface of the cells which may contain nuclear antigens and proteins which normally are retained within the plasma membrane1. The consequences are manifold. These "new antigens" may stimulate the production of autoantibodies, which in the predisposed individual may lead to clinical autoimmunity. A majority of the produced antibodies are polyreactive and may recognize nuclear and phospholipid antigens2. Should ischemia occur in sufficient magnitude, then naturally occurring crossreactive antibodies, anti-DNA or antibodies against other nuclear or phospholipid antigens will be engaged, activate complement, and facilitate local organ and, as we will discuss below, remote organ damage3. It should be noted that some of these autoantibodies, particularly those of the IgM class may counteract the action of others which are pathogenic4.
- Received February 7, 2015.
- Accepted February 11, 2015.