Implications of the Innate Immune Response in Tuberculosis and Cardiac Allograft Vasculopathy

Abstract

Reactivation of latent tuberculosis (TB) in HIV-infected individuals has arisen as a major contributor to early death in areas where TB and HIV overlap. CD4+ T cells are the targets of HIV, leading to insufficient IFN-γ to control disease. In the first section of this thesis I tested natural extracts to synergize with IFN-γ to control Mtb growth. Infected macrophages were treated with the extracts and IFN-γ. Although the extracts showed no synergy with IFN-γ, this model of ex vivo infection could provide a template for future study. The second section investigated the contribution of pre-existing atherosclerosis to the development of allograft vasculopathy (AV). Aortas from ApoEKO mice bearing an atherosclerotic lesion were transplanted into fully disparate recipients, treated with Cyclosporin A and changes in size and structure were analyzed. The results support our hypothesis that by 7d changes in the atherosclerotic lesion post-transplant set the stage for AV.