Chronic type I IFN signaling redirects autophagy from a general nutrient‑recycling program to a selective mitophagy‑focused response, thereby exhausting the bulk autophagic flux reserve and precipitating immune senescence. It's known that sustained IFN‑I receptor signaling activates STAT1‑dependent transcription of the autophagy receptor NIX (BNIP3L) and concurrently suppresses ULK1 serine‑757 phosphorylation via mTORC1 inhibition, creating a molecular bias that prioritizes mitochondrial clearance over bulk cargo degradation. In aged T cells, this bias depletes the pool of autophagosomes available for non‑mitophagic substrates, leading to accumulation of protein aggregates and lipid droplets that impair metabolic flexibility and proliferative capacity. Blocking IFN‑I signaling with an anti‑IFNAR1 antibody should restore ULK1‑mediated bulk autophagy initiation without affecting NIX‑driven mitophagy, measurable as increased LC3‑II turnover in response to rapamycin and decreased p62 accumulation, while mitophagy flux (measured by mitochondrial‑Keima) remains unchanged. Restored bulk flux is predicted to rescue glycolytic reserve and NAD+ levels, improving T cell proliferation in vitro and enhancing vaccine‑induced antibody titers in aged mice. Conversely, genetic overexpression of NIX in young T cells under low IFN conditions should mimic the aged phenotype by selectively consuming flux reserve, causing bulk autophagy deficiency and metabolic exhaustion despite intact mitophagy. These predictions don't rely on ambiguous readouts; they are falsifiable: if IFNAR1 blockade fails to increase bulk LC3‑II turnover or if NIX overexpression does not reduce bulk autophagy flux despite unchanged mitophagy, the hypothesis is refuted. Experimental validation would involve isolating CD4+ T cells from young (3‑month) and aged (24‑month) mice, treating them with anti‑IFNAR1 or isotype control for 48 h, then assessing autophagic flux using bafilomycin A1‑blocked LC3‑II immunoblotting and p62 degradation. Parallel mitophagy assays would employ mitochondrially targeted Keima or mt‑Cherry‑GFP reporters to ensure that selective mitochondrial clearance remains constant across conditions. Metabolic profiling would quantify extracellular acidification rate (ECAR) and oxygen consumption rate (OCR) via Seahorse analyzer, focusing on spare respiratory capacity and glycolytic reserve. NAD+ levels would be measured by enzymatic cycling assay, and proliferative capacity gauged by CFSE dilution after anti‑CD3/CD28 stimulation. In vivo, aged mice receiving anti‑IFNAR1 weekly for four weeks prior to immunization with a model antigen (OVA) would be evaluated for germinal center B cell frequency and serum IgG titers. A complementary gain‑of‑function approach would transduce young T cells with a lentiviral NIX construct, confirming that forced NIX expression alone reduces bulk autophagy flux (LC3‑II turnover) without altering mitophagyKeima signal, and reproduces the metabolic exhaustion phenotype. Statistical analysis would use two‑way ANOVA with post‑hoc Tukey tests; a p‑value <0.05 would be considered significant. If the data conform to these predictions, we'll see that chronic IFN‑I signaling acts as a molecular switch that skews autophagy selectivity, converting a protective rationing system into a driver of flux reserve depletion and immune aging.