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SCS macrophages suppress melanoma by restricting tumor-derived vesicle–B cell interactions

2016· article· en· 346 citations· W2309770165 on OpenAlex· 10.1126/science.aaf1328

Why is this work in the frame?

A frame that forgets how it found something cannot be audited. These are the routes that admitted this work.

Canadian funderA Canadian agency funded it. The work may carry no Canadian affiliation at all.

No Canadian affiliation. An affiliation-only frame — the usual design — would never have seen this work. It is one of the works that make the case for inverting the frame.

Machine scores (provisional)

Baseline scores from an immature model (maturity gate not passed, 7 training rounds). Scores rank; they never assert a category.

The two teacher heads of the student model, read on this work. A score orders the frame for review; it never asserts a category, and the validation status ships verbatim with every row.

Opus teacher head0.006
GPT teacher head0.248
Teacher spread
0.242 · how far apart the two teachers sit on this one work
Validation status
score_only:v0-immature-baseline · verbatim from the scoring run: score_only means the number may rank works, and no category label ships from it

Abstract

Tumor-derived extracellular vesicles (tEVs) are important signals in tumor-host cell communication, yet it remains unclear how endogenously produced tEVs affect the host in different areas of the body. We combined imaging and genetic analysis to track melanoma-derived vesicles at organismal, cellular, and molecular scales to show that endogenous tEVs efficiently disseminate via lymphatics and preferentially bind subcapsular sinus (SCS) CD169(+) macrophages in tumor-draining lymph nodes (tdLNs) in mice and humans. The CD169(+) macrophage layer physically blocks tEV dissemination but is undermined during tumor progression and by therapeutic agents. A disrupted SCS macrophage barrier enables tEVs to enter the lymph node cortex, interact with B cells, and foster tumor-promoting humoral immunity. Thus, CD169(+) macrophages may act as tumor suppressors by containing tEV spread and ensuing cancer-enhancing immunity.

Fetched live from OpenAlex and de-inverted. Abstracts are not stored in this database: the inverted indexes are 8.6 GB of the frame’s 9.3 GB of text, and the host has 13 GB free.

The record

Venue
Science
Topic
Extracellular vesicles in disease
Field
Biochemistry, Genetics and Molecular Biology
Canadian institutions
Funders
National Institute of Biomedical Imaging and BioengineeringNational Institute of Neurological Disorders and StrokeNational Institute of Allergy and Infectious DiseasesBoehringer Ingelheim FondsDeutsche ForschungsgemeinschaftCanadian Institutes of Health ResearchNational Cancer InstituteNational Institutes of HealthNational Institute of Diabetes and Digestive and Kidney DiseasesEuropean Molecular Biology Organization
Keywords
LymphImmune systemMelanomaExtracellular vesiclesCancer researchPopulationTumor cellsTumor microenvironmentMicrovesiclesBiologyImmunologyCell biologyMedicinePathologyGenetics
Has abstract in OpenAlex
yes