Abstract
Proteasomes and lysosomes constitute the major cellular systems that catabolize proteins to recycle free amino acids for energy and new protein synthesis. Tripeptidyl peptidase II (TPPII) is a large cytosolic proteolytic complex that functions in tandem with the proteasome-ubiquitin protein degradation pathway. We found that autosomal recessive TPP2 mutations cause recurrent infections, autoimmunity, and neurodevelopmental delay in humans. We show that a major function of TPPII in mammalian cells is to maintain amino acid levels and that TPPII-deficient cells compensate by increasing lysosome number and proteolytic activity. However, the overabundant lysosomes derange cellular metabolism by consuming the key glycolytic enzyme hexokinase-2 through chaperone-mediated autophagy. This reduces glycolysis and impairs the production of effector cytokines, including IFN-γ and IL-1β. Thus, TPPII controls the balance between intracellular amino acid availability, lysosome number, and glycolysis, which is vital for adaptive and innate immunity and neurodevelopmental health.
Original language | English |
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Pages (from-to) | 1578-90 |
Number of pages | 13 |
Journal | Cell |
Volume | 159 |
Issue number | 7 |
DOIs | |
Publication status | Published - 18 Dec 2014 |
Keywords
- Adaptive Immunity
- Amino Acid Sequence
- Aminopeptidases
- Animals
- Dipeptidyl-Peptidases and Tripeptidyl-Peptidases
- Female
- Glycolysis
- Humans
- Immunity, Innate
- Immunologic Deficiency Syndromes
- Lysosomes
- Male
- Models, Molecular
- Molecular Sequence Data
- Pedigree
- Proteolysis
- Sequence Alignment
- Serine Endopeptidases