ReviewFrontiers in immunology2026
A proposed convergent molecular chain linking senescence, cancer, and chronic infection to a correctable failure of dendritic cell instruction.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Three convergent phenomena in biomedical research have lacked a unified mechanistic explanation: the dendritic cell dysfunction of aging, the immune evasion of cancer, and the tolerogenic bias of chronic infection. Each is characterized by failure of type 1 conventional dendritic cell (cDC1) instruction and loss of its bioactive IL-12p70 output. Hypothesis: We propose that these three phenomena share a single molecular cause: sustained silencing of IRF8 by a four-step chain. SASP cytokines activate STAT3 in hematopoietic progenitors; STAT3 recruits DNMT1 and EZH2 to the IRF8 locus; dual DNA and histone methylation installs a bistable silencing state with no stable intermediate; IL-12 transcription and cDC1 instruction collapse. Each step is individually established in the literature. Their assembly is a deduction rather than a new discovery. Proposed correction: A cDC1 manufactured ex vivo outside the SASP-STAT3 field, the α-type-1 polarized dendritic cell (α-DC1), is not subject to the chain and produces IL-12p70 at supraphysiological concentrations. If the chain is correct, α-DC1 administration should restore endogenous IRF8 expression, re-enable cDC1 surveillance, and decelerate biological aging as measured by DunedinPACE. We outline the mechanism, testable predictions, and falsification criteria.
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