Evidence map›Paper›PMID 41993385›Full record

ArticlebioRxiv : the preprint server for biology2026

Overlapping MHC class I/II Epitopes Program cDC1-like Differentiation of Monocyte-Derived Dendritic Cells via mTORC1 Signaling Inhibition.

S B Amanya, A Murthy, N Bisht, Z N Bullock, K J Ernste, J Vasquez-Perez, W Liu, A Trivedi, D Oyewole-Said, A Paul and 13 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

23 authors.

S B AmanyaDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.ORCID 0000-0001-6372-8910
A MurthyDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
N BishtDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
Z N BullockDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
K J ErnsteDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
J Vasquez-PerezDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
W LiuDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
A TrivediDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
D Oyewole-SaidDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
A PaulDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
L UmokoroDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
V AkhanovDepartment of Neuroscience, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
M SamuelDepartment of Neuroscience, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
Z ShiAdvanced Technologies Core, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
M H NguyenAdvanced Technologies Core, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
S HuangAdvanced Technologies Core, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
M JeongSingle cell Genomics Core, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
P IakovaDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030.
K A JainDepartment of Epigenetics and Molecular Carcinogenesis, The University of Texas M.D. Anderson Cancer Center, Houston, TX 77030.
K PhamGenomic and RNA Profiling Core, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
D C KraushaarGenomic and RNA Profiling Core, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
V KonduriDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.
W K DeckerDepartment of Pathology and Immunology, Comprehensive Cancer Center, Baylor College of Medicine, Houston, TX 77030.

Funding

Tumor BiologyP30CA125123 · NCI · BAYLOR COLLEGE OF MEDICINE · PI Suzanne AW Fuqua · 2007 to 2026
$73.9M
Regulation of Innate Dendritic Cell CTLA-4R01AI127387 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI WILLIAM Karl DECKER · 2017 to 2026
$3.9M
Innate DC Govern TH Polarization through the Novel Regulator AIMp1R01AI153326 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI DECKER, WILLIAM KARL · 2021 to 2024
$2.3M
High Throughput Genomic Sequencer at BCM Core FacilityS10OD023469 · OD · BAYLOR COLLEGE OF MEDICINE · PI CHEN, RUI · 2017 to 2017
$600k
High Memory High-Performance Computer Cluster for Biomedical ResearchS10OD032185 · OD · BAYLOR COLLEGE OF MEDICINE · PI HILSENBECK, SUSAN G. · 2022 to 2022
$596k
Single Cell Spatial Transcriptomics Shared Instrument at the BCM Core FacilityS10OD032189 · OD · BAYLOR COLLEGE OF MEDICINE · PI CHEN, RUI · 2022 to 2022
$304k
NCI NIH HHS P30 CA125123NIAID NIH HHS R01 AI127387NIAID NIH HHS R01 AI153326NIH HHS S10 OD023469NIH HHS S10 OD032185NIH HHS S10 OD032189
6 · The paper itself

Abstract

Viral infection polarizes monocyte-derived dendritic cells (moDC) to initiate type 1 immunity. The availability of overlapping (homologous) MHC class I and II epitopes, an occurrence frequently and primarily associated with intracellular infection, significantly enhances this process; however, the underlying mechanism(s) are unclear. We demonstrate that moDC loaded with homologous MHC epitopes acquire a cDC1-like phenotype in a process governed by mTORC1. mTORC1 pathway inhibition leads to NF-κB-mediated expression of IL-12 and other type I immune polarizing genes. The observed cDC1-like gene signature was also significantly enhanced in clinical moDC vaccine products made through methodologies that enforced class I and II antigenic homology. Collectively, these findings reveal a novel and previously unrecognized mechanism of immune governance that might also be exploited in cancer immunotherapy.

Indexed as

cancer immunotherapyimmune regulationmajor histocompatibility complexmonocyte-derived dendritic cellType 1 conventional dendritic cellType 1 immunity

Identifiers

PMID41993385
PMCPMC13082029

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.