FH and Autoimmunity: Importantly, FH can bind to molecules that become exposed on cells during apoptosis (and necrosis), including DNA, histones and annexin II (and possibly the altered glycocalyx), where it is believed that this serves to minimize the downstream pro-inflammatory effects of complement activation and the release of autoantigens that would trigger autoimmunity [62, 64, 68, 69]; FH binding may also compensate for the loss of some membrane-bound inhibitors of complement.