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@alicefrolov.bsky.social Sep 28, 2026, 5:31 PM

Weakening of the DC–T Cell Immunological Synapse with Age

I am sharing a data visualization from ongoing conceptual work on age-associated remodeling.

#Immunosenescence #DendriticCells #ImmunologicalSynapse #TCellActivation #Costimulation #LigandReceptorInteractions

Weakening of the DC–T Cell Immunological Synapse with Age

I am sharing a data visualization from ongoing conceptual work on age-associated remodeling of dendritic cell–T cell communication at the immunological synapse. The figure, "Weakening of the DC–T Cell Immunological Synapse with Age," is rendered as a curved bipartite flow map (ligand-receptor arc diagram), with dendritic cell ligands on the left axis and cognate T cell receptors on the right. Arc width and opacity encode simulated signaling strength, contrasted between young and aged tissue states.

I want to be explicit that the underlying values are simulated. They are not drawn from a single empirical dataset but are parameterized to reproduce trends consistently reported in the immunosenescence literature. The visualization is intended as a mechanistic scaffold for discussion rather than as primary evidence.

The mapped interactions include the peptide-MHC Class II to TCR-CD3 axis, the costimulatory CD80/CD86 to CD28 pair, CD40 to CD40L feedback, ICAM-1 to LFA-1 adhesion, and inhibitory PD-L1 to PD-1 signaling. In the aged condition, the diagram depicts attenuated pMHCII–TCR and CD80/86–CD28 arc weights, consistent with reduced antigen presentation efficiency and diminished costimulatory competence in aged DCs. Concurrently, the PD-L1–PD-1 arc is broadened, reflecting the shift toward inhibitory tone described in exhausted and senescent T cell compartments. ICAM-1–LFA-1 attenuation is included to represent reported deficits in synapse stability and conjugate formation.

The composite effect illustrated here is a quantitative and qualitative degradation of productive synaptic signaling, favoring incomplete T cell priming and skewed activation thresholds. I would welcome critique on the ligand-receptor pair selection and on plausible weighting priors that could later be constrained with single-cell interactome or spatial proteomic data.

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