CD28 and myocardial infarction: Animal studies indicated that depletion of Treg after MI leads to a loss of regulation of the immune system, which, in turn, triggers and amplifies an exaggerated inflammatory response, thus worsening LV remodeling; as confirmation, Treg injection was found to decrease infarct size and improve cardiac function after MI [92] and activation of Treg by superagonistic anti-CD28 monoclonal antibody administered 2 days after MI improved healing and survival [112].