A single peripheral dose of human monoclonal antibody A6 protected mice from lethal Australian bat lyssavirus after CNS invasion, with cryo-EM defining a new prefusion-specific glycoprotein epitope — but evidence rests on small mouse groups (n=3–8) and an attenuated mutant that arose spontaneously, so the inflammation-versus-lethality dissociation is suggestive rather than proven.
ABLV monoclonal antibody review →A CaCO3/protamine nanoparticle delivered CRISPR plasmids to tumor nuclei, achieving ~40% β-catenin knockout, lowering PD-L1, and increasing CD8+ T cell proliferation in vitro — all findings are cell-culture only, with no animal or off-target sequencing data.
Aptamer-functionalized CRISPR immunotherapy study →Stereo-XCR-seq retrieves paired TCR/BCR sequences at subcellular spatial resolution and was demonstrated across cancer and Crohn's disease samples — but the work is an unreviewed preprint whose human claims rest on only three patients and proprietary platforms.
Stereo-XCR-seq spatial repertoire preprint →The hypothesis that impaired antigen presentation plus reduced granzyme clearance permits defective viral genomes to persist in gut tissue remains untested — no supplied records contain gut biopsy, immune effector, or persistence data, and defective genomes may present no antigens at all, making the mechanism internally inconsistent. Rated 25% likely (BGPT Odds of True).
PASC defective-genome persistence analysis →Tumor-cell CD24 suppressed macrophage clearance of colorectal cancer cells in zebrafish xenografts (~70–80% vs ~20% clearance upon knockout), consistent with a Siglec-type checkpoint — but the molecular receptor identity is unvalidated and all mechanistic work used one isogenic cell pair in larvae.
CD24 innate checkpoint zebrafish study →Pre-vaccination neutralization titers independently predicted reduced COVID-19 risk in the CoVPN 3008 cohort (HR 0.46 per 10-fold rise, 95% CI 0.28–0.75), with vaccine-only protection waning by 92 days — a rigorous case-cohort design, though limited to well-controlled HIV, mostly African participants, and no placebo arm.
CoVPN 3008 immune correlate study →A narrative review maps cytokine, antibody, and NK-engager approaches with striking single-arm signals (N-803+BCG 71% complete response; AFM13+NK 100% response in CD30+ lymphoma) — but undisclosed literature selection and a disclosed industry conflict weaken confidence, and its value lies in the failure-mode taxonomy rather than efficacy claims.
NK cell cytotoxicity therapeutic review →Bacteria-triggered chemokines (CCL5, CXCL9/10) recruit T cells into colorectal tumors, supported across human cohorts, organoids, and xenografts — but the human evidence is correlational, the microbiota cohort was small (n=27), and no 16S data accession was deposited.
Gut microbiota T cell trafficking study →An 88-gene pan-cancer signature defines CCR8+ effector Tregs, and TCR sequencing implicates lymph nodes — not intratumoral differentiation — as their source, predicting why anti-CCR8 depletion may be transient; the decisive clonal evidence comes from only three patients with inferential, not experimental, lineage tracing.
CCR8+ Treg atlas study →Two negative-feedback motifs encode prior stimulus history at hours scale, explaining why LPS but not IL-1β induces lasting feedback — validated with pharmacology, genetics, and >10,000 single-cell traces, though the model is an immortalized fibroblast line and the preprint is not yet peer-reviewed.
NF-κB memory dynamics preprint →Human endogenous retrovirus profiles stratify ME/CFS subgroups in one small cohort, and complement activation is independently observed post-exercise, but no study has jointly measured both — the predictive claim is untested, rated 35% likely (BGPT Odds of True), with HERV signals plausibly acting as proxies for primed innate immune circuits rather than causal viral elements.
HERV microclot hypothesis analysis →A self-critical review argues triptolide could shift from blunt immunosuppression toward immune reprogramming (Th17/Tfh suppression, Treg promotion), but translation is blocked by mechanism-based hepatic, renal, and reproductive toxicity — with prior derivative programs failing on the covalent warhead itself, not formulation.
Triptolide immune reset review →In MISTRG6 humanized mice, wild-type endothelial cells drove rejection of 3D-printed human skin while CRISPR MHC I/II-knockout endothelial cells were protected (histologic score 0.20 vs 1.79, p=0.0006) — but the "sufficient" claim overreaches because non-endothelial MHC was intact, and knockout group sizes were 3–5 mice.
3D-printed skin graft rejection study →Estradiol plus progesterone together decrease let-7f, derepressing IL-23R and raising IL-17A in T helper 17 cells — the first mechanistic link between ovarian hormones and severe-asthma sex bias, though based on small single-center cohorts and with the upstream hormone-to-microRNA mechanism undefined.
Sex hormone IL-17A asthma study →Aging CD8 T cells lose CD8 expression and CD226 effector identity through IL-4/IL-13–driven cytokine signaling, mechanistically paralleling tumor-induced CD8 dysfunction — the convergence is proposed from established pathway evidence, and causal validation experiments remain designs rather than completed studies.
Inflammaging CD8 remodeling plan →A CRISPR screen of 1,213 RNA-binding proteins found YTHDF2 promotes plasma cell accumulation in vivo (3–5-fold reductions without it) and the CCR4-NOT complex acts as a shared deadenylase hub — high-quality resource work, but only YTHDF2 was validated in animals and the m6A-dependence of its effect is unresolved.
Plasma cell RBP CRISPR screen →Antiphospholipid antibodies drive neutrophils to release NETs via ROS and TLR-4 signaling, promoting thrombin generation in a DNase-sensitive manner — a landmark 2015 mechanism study with rigorous controls, though the clinical correlation for arterial thrombosis was modestly powered (P=0.04) and no in vivo APS model data were included.
NETosis in antiphospholipid syndrome study →CXCR6+ cytotoxic CAR CD4+ T cells accumulate in cerebrospinal fluid during neurotoxicity, with CSF CXCL16 correlating with severity across grades 1–4 — multi-modal and internally consistent, but based on 11 patients, disease-mismatched controls, and one postmortem brain, leaving causality open.
CAR-T ICANS CXCL16 study →A single anchor substitution (S598 Q600Y) raised epitope thermal stability by ~10°C, primed ~100-fold higher-avidity T cells, and abolished viral escape in persistently infected mice — a rare complete causal chain from atomic structure to population protection, though demonstrated only in an inbred mouse coronavirus model.
Heteroclitic epitope design study →A released catalog of 26,106 public CMV-associated TCRβ clonotypes achieved strong held-out diagnostic performance (AUROC 0.96–0.97) — but it is an unreviewed corporate-authored preprint, clustering thresholds are admittedly arbitrary, and only 1.8% of the public response has assigned antigen specificity.
Public CMV TCR catalog preprint →An early review accurately predicted tumor PD-L1 as an evasion driver, PD-1 blockade to rescue exhausted T cells, and autoimmunity risk — historically validated within a decade, though as a narrative review it generated no primary data and relied partly on limited reagents.
PD-L1/PD-1 exhaustion review →BCG vaccination at birth improved neonatal mouse survival to cecal-slurry sepsis from 44% to 82% (p<0.01), with protection depending on timing (day 1 > day 4) — strong litter-randomized design with public data, but bacterial burden was never quantified and causality remains correlational.
Neonatal BCG trained immunity study →MINFLUX nanoscopy resolved 35–249 NLRC4 discs per ASC speck in primary human macrophages, with sparse hNAIP content (~30% colocalization) suggesting hNAIP acts as a transient nucleator rather than a stoichiometric component — but sample sizes were tiny (22 cells, 16 specks) and no loss-of-function perturbation tested causality.
MINFLUX inflammasome imaging study →Hepatitis C virus upregulates the host microRNA miR-373, which directly targets JAK1 and IRF9 to blunt STAT1 phosphorylation and antiviral signaling — a complete mechanistic chain with reciprocal gain/loss experiments, but resting on two hepatocyte donor lines and small biopsy samples.
HCV miR-373 JAK/STAT study →Non-classical monocytes use α4β7 to home to the gut and differentiate into repair macrophages, with vedolizumab blocking homing and delaying murine colonic wound closure (~20%) — a complete mechanistic chain including lymphocyte-independence, but no public data deposit and the perioperative clinical claim rests on hypothesis only.
α4β7 monocyte wound healing study →Human Langerhans cells fail to phosphorylate ERK after TLR2/3/7/8 stimulation yet drive Th2-biased responses, dismantling the ERK→Th2 dogma from monocyte-derived dendritic cells — well-controlled six-replicate work, but the actual ERK-independent Th2 mechanism remains unidentified.
Langerhans cell ERK-independent Th2 study →Myeloid Brd4 deletion protected high-fat diet-fed mice from colonic inflammation by suppressing NF-κB–dependent enhancer RNA at a shared Ccr2/Ccr5 enhancer, reducing macrophage infiltration and endotoxemia — mechanistically layered but mouse-only, male-only, with modest sample sizes and no eRNA rescue experiment.
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