Evidence map›Paper›PMID 42612021›Full record

ArticleOncoimmunology2026

Myeloid-derived MIF is a central regulator of MDSC-driven T-cell dysfunction in head and neck squamous cell carcinoma.

Suvekshya Shrestha, Felipe Lamenza, Natalie Kazmierowicz, Kishan Kumar Nyati, Sushmitha Jagadeesha, Ravi Ramalingam, Reegan Kehres, Puja Upadhaya, Arham Siddiqui, Shaheer Masood and 3 more

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In one paragraph

Article in Oncoimmunology, 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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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

13 authors.

Suvekshya ShresthaDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Felipe LamenzaDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Natalie KazmierowiczDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Kishan Kumar NyatiDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Sushmitha JagadeeshaDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Ravi RamalingamDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Reegan KehresDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Puja UpadhayaDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Arham SiddiquiDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Shaheer MasoodDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Massar YadeDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Sonali DasariDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.
Steve OghumuDepartment of Pathology, Pelotonia Institute for Immuno-Oncology, The Ohio State University Comprehensive Cancer Center, College of Medicine, The Ohio State University Wexner Medical Center, Columbus, OH, USA.ORCID 0000-0001-5177-0652

Funding

X chromosome inactivation in sex disparities to substance use disorderDP1DA054344 · NIDA · OHIO STATE UNIVERSITY · PI Steve Onyeka Oghumu · 2021 to 2026
$2.4M
The oral glucocorticoid system in oral carcinogenesis and its modulation for improved treatment outcomesR01DE033906 · NIDCR · OHIO STATE UNIVERSITY · PI Steve Onyeka Oghumu · 2024 to 2026
$1.9M
NIDA NIH HHS DP1 DA054344NIDCR NIH HHS R01 DE033906
6 · The paper itself

Abstract

backgroundHead and neck squamous cell carcinoma (HNSCC) exhibits a profoundly immunosuppressive tumor microenvironment (TME) enriched for myeloid-derived suppressor cells (MDSCs), regulatory T cells (Tregs), and dysfunctional CD8⁺ T cells, limiting therapeutic benefit from immune checkpoint blockade. Macrophage migration inhibitory factor (MIF) is elevated in HNSCC and linked to poor outcomes, yet the cellular source and functional role of tumor-promoting MIF in shaping antitumor immunity remain unclear.

methodsWe used a myeloid-specific MIF knockout mouse (mMIF KO) in an orthotopic MOC2 HNSCC model and evaluated immune function using

resultsMyeloid-restricted MIF deletion significantly reduced tumor growth and increased CD8⁺ T cell infiltration, accompanied by reduced CTLA4, TIGIT, and TIM3 expression, with elevated PD1 consistent with antigen-engaged effector activation. High-dimensional immune profiling revealed expansion of cytotoxic CD8⁺ T cell states (GranzymeB

conclusionsThese findings identify myeloid-derived MIF as a central regulator of the MDSC-Treg-CD8⁺ axis in HNSCC and support myeloid-targeted MIF inhibition as a strategy to reprogram the TME and enhance responses to immune checkpoint blockade.

Indexed as

Carcinoma, Squamous CellCD8-Positive T-LymphocytesHead and Neck NeoplasmsIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMyeloid-Derived Suppressor CellsAnimalsCell Line, TumorCoculture TechniquesHumansMiceMice, KnockoutSquamous Cell Carcinoma of Head and NeckT-Cell ExhaustionT-Lymphocytes, RegulatoryTumor MicroenvironmentIntramolecular OxidoreductasesMacrophage Migration-Inhibitory FactorsMif protein, mouseHNSCCimmunotherapyMDSCsMIFT cell exhaustionTregstumor microenvironment

Identifiers

PMID42612021
PMCPMC13488472

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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.