Evidence map›Paper›PMID 30944253›Full record

ArticleJCI insight2019

Inhibiting myeloid-derived suppressor cell trafficking enhances T cell immunotherapy.

Lillian Sun, Paul E Clavijo, Yvette Robbins, Priya Patel, Jay Friedman, Sarah Greene, Rita Das, Chris Silvin, Carter Van Waes, Lucas A Horn and 5 more

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 168 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
168citing papers in PubMed, 1 pooled it
11.6field-weighted citation impact, top 1% of its field
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

168 citing papers in PubMed, 1 synthesis or guideline pooled it, 228 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Leveraging Microphysiological Systems to Facilitate Neutrophil-Based Cancer Immunotherapy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  10. Alveolar macrophage-neutrophil crosstalk in acute lung injury: mechanisms, feedback loops, and therapeutic opportunities.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Review
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  13. RNAi-mediated p38δ silencing mitigates anthracycline cardiotoxicity in female mice.American journal of physiology. Heart and circulatory physiology · 2026
    Article
  14. Review
  15. Article
  16. Inhalable perfluorocarbon RNA nanocapsules overcome biological barriers to treat lung metastases.Journal of controlled release : official journal of the Controlled Release Society · 2026
    Article
  17. Neutrophil extracellular traps in cancer.Nature reviews. Cancer · 2026
    Review
  18. Article
  19. Review
  20. Loss of SETD2-mediated H3K36me3 Drives CD8Research (Washington, D.C.) · 2026
    Article

108 more citing papers are in PubMed but not listed here.

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

15 authors at 5 institutions in 2 countries.

Lillian SunTranslation Tumor Immunology Program and.
Paul E ClavijoTranslation Tumor Immunology Program and.
Yvette RobbinsTranslation Tumor Immunology Program and.
Priya PatelTranslation Tumor Immunology Program and.
Jay FriedmanTranslation Tumor Immunology Program and.
Sarah GreeneTranslation Tumor Immunology Program and.
Rita DasTumor Biology Section, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, USA.
Chris SilvinTumor Biology Section, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, USA.
Carter Van WaesTumor Biology Section, National Institute on Deafness and Other Communication Disorders, NIH, Bethesda, Maryland, USA.
Lucas A HornLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Jeffrey SchlomLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Claudia PalenaLaboratory of Tumor Immunology and Biology, Center for Cancer Research, National Cancer Institute, NIH, Bethesda, Maryland, USA.
Dean MaedaSyntrix Pharmaceuticals, Auburn, Washington, USA.
John ZebalaSyntrix Pharmaceuticals, Auburn, Washington, USA.
Clint T AllenTranslation Tumor Immunology Program and.
National Center for Tumor Diseases · DENational Cancer Institute · USNational Institute on Deafness and Other Communication Disorders · USSyntrix Biosystems (United States) · USJohns Hopkins University · US

Funding

Characterization and Enhancement of Anti-Tumor Immune Responses in Head and Neck CancerZIADC000087 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI ALLEN, CLINT · 2015 to 2022
$13.5M
Novel Targets for Vaccine TherapyZICBC010937 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI PALENA, CLAUDIA · 2010 to 2022
$13.2M
Intramural NIH HHS ZIA DC000087
6 · The paper itself

Abstract

Recruitment of myeloid-derived suppressor cells (MDSCs) into tumors induces local immunosuppression in carcinomas. Here, we assessed whether SX-682, an orally bioavailable small-molecule inhibitor of CXCR1 and CXCR2, could block tumor MDSC recruitment and enhance T cell activation and antitumor immunity following multiple forms of immunotherapy. CXCR2+ neutrophilic MDSCs (PMN-MDSCs) were the most abundant myeloid cell subset within oral and lung syngeneic carcinomas. PMN-MDSCs demonstrated greater suppression of tumor-infiltrating lymphocyte killing of targets compared with macrophages. SX-682 significantly inhibited trafficking of PMN-MDSCs without altering CXCR2 ligand expression. Trafficking of CXCR1+ macrophages was unaltered, possibly due to coexpression of CSF1R. Reduced PMN-MDSC tumor infiltration correlated with enhanced accumulation of endogenous or adoptively transferred T cells. Accordingly, tumor growth inhibition or the rate of established tumor rejection following programed death-axis (PD-axis) immune checkpoint blockade or adoptive cell transfer of engineered T cells was enhanced in combination with SX-682. Despite CXCR1/2 expression on tumor cells, SX-682 appeared to have little direct antitumor effect on these carcinoma models. These data suggest that tumor-infiltrating CXCR2+ PMN-MDSCs may prevent optimal responses following both PD-axis immune checkpoint blockade and adoptive T cell transfer therapy. Abrogation of PMN-MDSC trafficking with SX-682 enhances T cell-based immunotherapeutic efficacy and may be of benefit to patients with MDSC-infiltrated cancers.

Indexed as

AnimalsAntineoplastic Agents, ImmunologicalCarcinomaCell Line, TumorCell MovementCombined Modality TherapyDisease Models, AnimalHumansImmune ToleranceImmunotherapy, AdoptiveLung NeoplasmsLymphocytes, Tumor-InfiltratingMiceMouth NeoplasmsMyeloid-Derived Suppressor CellsNeutrophilsAntineoplastic Agents, ImmunologicalCxcr2 protein, mouseReceptors, Interleukin-8AReceptors, Interleukin-8BImmunotherapyOncology

Identifiers

PMID30944253
PMCPMC6483637
OpenAlexW2935366665

What OpenQuestion holds

Textmetadata
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.