Autophagy is a ubiquitous eukaryotic cytoplasmic quality and quantity control 
pathway. The role of autophagy in cytoplasmic homeostasis seamlessly extends to 
cell-autonomous defense against intracellular microbes. Recent studies also 
point to fully integrated, multitiered regulatory and effector connections 
between autophagy and nearly all facets of innate and adaptive immunity. 
Autophagy in the immune system as a whole confers measured immune responses; on 
the flip side, suppression of autophagy can lead to inflammation and tissue 
damage, as evidenced by Crohn's disease predisposition polymorphisms in 
autophagy basal apparatus (Atg16L) and regulatory (IRGM) genes. Polymorphisms in 
the IRGM gene in human populations have also been linked to predisposition to 
tuberculosis. There are several areas of most recent growth: first, links 
between autophagy regulators and infectious disease predisposition in human 
populations; second, demonstration of a role for autophagy in infection control 
in vivo in animal models; third, the definition of specific antiautophagic 
defenses in highly evolved pathogens; and fourth, recognition of connections 
between the ubiquitin system and autophagy of bacteria (and interestingly 
mitochondria, which are incidentally organelles of bacterial evolutionary 
origin) via a growing list of modifier and adapter proteins including 
p62/SQSTM1, NDP52, Atg32, Parkin, and Nix/BNIP3L.