What question did this study set out to answer?

To present a theoretical framework for enhancing immune surveillance using engineered T-cell variants across distinct biophysical channels.

May 4, 2026Open Access

DQIS — Distributed Quantum-Inspired Immune Surveillance: A Theoretical Framework for Multi-Channel Independent Immune Surveillance Against Tumor Evasion

Key Points

To present a theoretical framework for enhancing immune surveillance using engineered T-cell variants across distinct biophysical channels.
Proposed five engineered T-cell variants operating on metabolic, mechanical, bioelectric, epigenetic, and topological channels.
Utilized a distributed consensus protocol to coordinate T-cell actions.
Analyzed empirical theta measurements from single-cell RNA sequencing data for tumors.
Showed a significant 15.5× increase in IPS signals in PDAC compared to normal pancreas, with a low false alarm rate (P=0.0003).
Reported T-α v3.0 module can effectively resolve self-activation issues with activation probabilities between 0.0003 and 0.002.
Demonstrated a theoretical efficacy ranging from 75× to 30,000× reductions in tumor escape rates with the proposed T-cell constructs.

Abstract

DQIS — Distributed Quantum-Inspired Immune Surveillance: Consolidated Framework v22. 0 This document presents DQIS — a theoretical framework proposing to augment natural immune surveillance with five engineered T-cell variants operating on orthogonal biophysical channels (metabolic, mechanical, bioelectric, epigenetic, topological), coordinated by a distributed consensus protocol. The core principle — borrowed from quantum cryptography — is that statistically independent verification channels reduce joint tumor escape probability multiplicatively. Version 22. 0 principal updates. Direct empirical θ measurement on real scRNA-seq data: GBM (GSE131928, 7, 911 cells) θ=0. 199 — reclassified from cold to hot, identical to melanoma; PDAC (GSE155698, 11, 448 cells) θ=1. 214 — confirmed cold for intrinsic biological reasons (normal pancreas θ=1. 107, GSE84133). Penetrance discovery: IPS signal 15. 5× in PDAC vs normal pancreas, 10. 1× in IPMN precancerous lesions — P (false alarm, N=1, 000 cells) =0. 0003. T-ζ-IPS module provides population-level PDAC detection without modifying existing constructs. T-α v3. 0 triple-AND-gate resolves self-activation (pᵢ=0. 0003–0. 002). PAA architecture resolves tonic signaling exhaustion (ε (10y) =0. 921, analytically proven). Operative efficacy claims (three-phase model). Phase 0 PoC: ~75× reduction using T-γ* + T-δ with existing approved technology. DQIS-3: ~360–980× (5–7 years). DQIS-5: ~5, 000–30, 000× (10–12 years). Theoretical ceiling ~4, 000, 000× (k=5 unanimous, θ=0) is non-operative and reported for completeness only. The framework is explicitly theoretical. Wet-lab experimental validation is the required next step. This document is structured as a foundation for academic discussion and a target for experimental falsification. Contact: dqis. research@proton. me Related documents: - Register of Scientific Objections v4. 0: https: //zenodo. org/records/19880166 - Addendum I — Temporal Stratification of Tail Dependence Risk: https: //zenodo. org/records/19877810

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