Vojo Deretic, Ph.D., is Chair of the Department of Molecular Genetics & Microbiology at the University of New Mexico School of Medicine. He received his undergraduate, graduate and postdoctoral education in Belgrade, Paris, and Chicago. Dr. Deretic's main contributions to science come from studies by his team on the role of autophagy in infection and immunity. His group is one of those that made the discovery that autophagic degradation is a major effector of innate and possibly adaptive immunity mechanisms for direct elimination of intracellular microbes (such as Mycobacterium tuberculosis).
The Deretic laboratory has shown that autophagy in mammalian cells plays not only a degradative role but that it also carries the task of unconventional secretion of immunologically active cytoplasmic proteins, such as IL-1beta and others. These proteins normally reside in the cytosol but exert their functions extracellularly. The latest studies in Dr. Deretic's laboratory show that a large family of proteins termed TRIMs, playing immune and other roles but with incompletely understood function(s), acts as autophagic receptor-regulators in mammalian cells. TRIMs organize autophagic machinery in mammalian cells to carry out a highly selective or "precision" autophagy of their targets.
A series of studies from Dr. Deretic's group show how the human immunity related GTPase IRGM works in autophagy by demonstrating IRGM's direct interactions with the core autophagy (ATG) factors, and their assembly and activation enabling them to carry out antimicrobial and anti-inflammatory autophagic functions of significance in tuberculosis and Crohn's disease.
The recent primary publications in Molecular Cell and in J. Cell Biol. Related to the above areas of study are available through these links: http://www.cell.com/molecular-cell/abstract/S1097-2765%2815%2900211-7; http://jcb.rupress.org/content/210/6/973. Recent comprehensive reviews by Deretic and colleagues that summarize the role of autophagy in immunity and inflammation can be found here: