Vojo Deretic, is distinguished professor and chair of the Department of Molecular Genetics and Microbiology at the University of New Mexico School of Medicine.

Deretic's group is one of those that made the discovery[7] that autophagic degradation is a major effector of innate and possibly adaptive immunity mechanisms for direct elimination of intracellular microbes (such as Mycobacterium tuberculosis[8][9][10]).

For example, as shown in a study [11] from the Deretic laboratory, SARS-CoV-2 inhibits the earliest stage of autophagosome formation in human cells known as the prophagophore or HyPAS.

[21] TRIMs play immune and other roles but with incompletely understood function(s), and the above cited work shows that they act as autophagic receptor-regulators in mammalian cells.

[22][19][23][24] A series of studies[18][25][26][27] from Deretic's group shows 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 downstream of PRRs: NOD1, NOD2, TLRs, RIG-I and inflammasome components, enabling them to carry out antimicrobial and anti-inflammatory autophagic functions of significance in tuberculosis and Crohn's disease.

A related line of studies shows that IRGM helps recruit a SNARE Syntaxin 17, which is also a target for phosphorylation and control by TBK1[28] and plays a role in both autophagy initiation and maturation.

It has recently been expanded to a large number of other SNAREs, with one specific subset characterized as driving lysosome biogenesis via a TGN-lysosome trafficking route.

[30] These studies have led to an unanticipated alternative model for how mammalian ATG8s work – by broadly interacting with and modulating SNAREs to redirect general intracellular membrane flow toward the organelles that converge upon the lysosomal-autolysosomal system.

Moreover, recent studies[29][30] show that mammalian ATG8s actually regulate lysosomal biogenesis, expanding or potentially revising their function that was originally restricted to be autophagosomal formation.

As mentioned above, atg8ylation and specific mATG8s (curiously, excluding LC3B) direct ESCRTs to complete autophagosmal closure and to maintain autophagic membranes in a sealed state.

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 cytoplasmic proteins.

[44] A comprehensive review with over 1,500 citations by Deretic and colleagues summarizes the role of autophagy in immunity and inflammation:[4] A more recent review[5] by Deretic in the Cell Press journal Immunity summarizes the role of autophagy in inflammation and how it affects various diseases, from autoimmunity to cancer, infections (including COVID-19), cardiovascular and liver diseases, neurodegeneration, diabetes and metabolic disorders.