Caveat: Monoclonal antibodies 20.1 and 103.2 bind all human BTN3A proteins and are not suited to study BTN3A1-specific features.

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.

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.

Who cites it

3 citing papers in PubMed.

1. Mechanisms and Functions of γδ T Cells in Tumor Cell Recognition.Current oncology (Toronto, Ont.) · 2025
   Review
2. Reply to Herrmann et al.: The BTN3A isoform BTN3A1 is responsible for phosphoantigen-induced Vγ9Vδ2 T cell activation.Proceedings of the National Academy of Sciences of the United States of America · 2023
   Article
3. γδ T cell-mediated cytotoxicity against patient-derived healthy and cancer cervical organoids.Frontiers in immunology · 2023
   Article

Corrections and comments

• Commented on by
  Reply to Herrmann et al.: The BTN3A isoform BTN3A1 is responsible for phosphoantigen-induced Vγ9Vδ2 T cell activation.2023
• Comment on
  Up-regulation of BTN3A1 on CD142022

Authors and funding

1 author.

Funding

No grant is acknowledged in the PubMed record.

Abstract

PubMed holds no abstract for this paper.

Indexed as