ER-phagy and mitophagy programs in human CD4+ memory T cells before and after activation
Morone, D.; Raimondi, A.; Molinari, M.
Show abstract
T lymphocytes can remain in a resting state for very long times. Encountering their cognate antigen triggers their activation, leading to an increase in cell size, proliferation, enhanced protein production, and secretion of signaling molecules. This activation and clonal expansion phase is followed by a contraction phase, with a reduction in cell size, eventually leading to cell death or progression to resting (memory) cells. Here, we show that human resting primary CD4+ memory T cells degrade endoplasmic reticulum (ER) and mitochondrial portions via ER-phagy and mitophagy, respectively. The temporary interruption of ER and mitochondria turnover coupled with a transient induction of the unfolded protein response results in the enlargement of the ER and cellular volume. Cell growth is stabilized and then reversed during the clonal expansion and contraction phases by the resumption of a catabolic phase characterized by the reactivation of ER-phagy and outer mitochondrial membrane (OMM)-phagy. Collectively, our data show that the maintenance and the activity of human CD4+ memory T cells rely on finely tuned execution of anabolic and catabolic programs that regulate mass and activity of the ER and mitochondria.
Matching journals
The top 9 journals account for 50% of the predicted probability mass.
Similar papers in this journal
Similar papers in this journal
- Microtubules restrict F-actin to the immune synapse via GEF-H1 to maintain polarity in lymphocytes 95%
- Allosteric Inhibition of the T Cell Receptor by a Designed Membrane Ligand 95%
- Actin-regulated Siglec-1 nanoclustering influences HIV-1 capture and virus-containing compartment formation in dendritic cells 95%
Similar papers in this journal
- ERLIN1/2 scaffolds bridge TMUB1 and RNF170 and restrict cholesterol esterification to regulate the secretory pathway 94%
- Characterizing control of memory CD8 T cell differentiation by BTB-ZF transcription factor Zbtb20 94%
- A genome-wide CRISPR functional survey of the human phagocytosis molecular machinery 94%
Similar papers in this journal
- TBK1 phosphorylation activates LIR-dependent degradation of the inflammation repressor TNIP1 94%
- Phagosome resolution regenerates lysosomes and maintains the degradative capacity in phagocytes 94%
- CHC22 clathrin mediates traffic from early secretory compartments for human GLUT4 pathway biogenesis 94%
Similar papers in this journal
- Galectin-9 binding to HLA-DR in dendritic cells controls immune synapse formation and T cell proliferation 96%
- Phosphatidylinositol-4-kinase IIα licenses phagosomes for TLR4 signaling and MHC-II presentation in dendritic cells 95%
- Extracellular vesicles released by keratinocytes regulate melanosome maturation, melanocyte dendricity and pigment transfer 95%
"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.