Evidence map›Paper›PMID 37001518›Full record

ArticleCell systems2023

Entropic analysis of antigen-specific CDR3 domains identifies essential binding motifs shared by CDR3s with different antigen specificities.

Alexander M Xu, William Chour, Diana C DeLucia, Yapeng Su, Ana Jimena Pavlovitch-Bedzyk, Rachel Ng, Yusuf Rasheed, Mark M Davis, John K Lee, James R Heath

Open access · greenAbstract read
In one paragraph

Article in Cell systems, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

4 citing papers in PubMed, 7 citations in OpenAlex.

  1. Review
  2. Limits on inferring T cell specificity from partial information.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
  3. Article
  4. Article
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

10 authors at 7 institutions in 1 country.

Alexander M XuInstitute for Systems Biology, Seattle, WA 98109, USA; Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, CA 91125, USA; Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA; Samuel Oschin Comprehensive Cancer Institute, Cedars-Sinai Medical Center, Los Angeles, CA 90048, USA. Electronic address: alexander.xu@cshs.org.
William ChourInstitute for Systems Biology, Seattle, WA 98109, USA; Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA 91125, USA; Keck School of Medicine, University of Southern California, Los Angeles, CA 91125, USA.
Diana C DeLuciaDivision of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
Yapeng SuInstitute for Systems Biology, Seattle, WA 98109, USA; Division of Chemistry and Chemical Engineering, California Institute of Technology, Pasadena, CA 91125, USA.
Ana Jimena Pavlovitch-BedzykComputational and Systems Immunology Program, Stanford University School of Medicine, Stanford, CA 94305, USA.
Rachel NgInstitute for Systems Biology, Seattle, WA 98109, USA.
Yusuf RasheedInstitute for Systems Biology, Seattle, WA 98109, USA.
Mark M DavisComputational and Systems Immunology Program, Stanford University School of Medicine, Stanford, CA 94305, USA; Institute for Immunity, Transplantation and Infection, Stanford University School of Medicine, Stanford, CA 94305, USA; Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Stanford University School of Medicine, Stanford, CA 94305, USA.
John K LeeDivision of Human Biology, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA; Division of Medical Oncology, Department of Medicine, University of Washington, Seattle, WA 98195, USA.
James R HeathInstitute for Systems Biology, Seattle, WA 98109, USA. Electronic address: jim.heath@isbscience.org.
Institute for Systems Biology · USCalifornia Institute of Technology · USFred Hutch Cancer Center · USHoward Hughes Medical Institute · USStanford University · USUniversity of Southern California · USUniversity of Washington Medical Center · US

Funding

Translational Bioimaging Core Shared ResourceP30CA015704 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI Eric Collisson · 1985 to 2026
$296.4M
UCLA Clinical Translational Science InstituteUL1TR001881 · NCATS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARLEEN F. BROWN, ARASH NAEIM · 2016 to 2026
$118.1M
Using a tonsil organoid system to probe conditions for the induction of protective antibody and T cell responses to influenza.U19AI057229 · NIAID · STANFORD UNIVERSITY · PI Mark Morris Davis · 2003 to 2026
$88.5M
TRANSCRIPTOME AND PROTEOME STRATIFICATION OF PROSTATE ADENOCARCINOMA PHENOTYPESP50CA097186 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PETER S NELSON · 2002 to 2026
$58.1M
The effects of immune-age on immune-response and the molecular mechanisms which drive itP01AI153559 · NIAID · STANFORD UNIVERSITY · PI DAVIS, MARK MORRIS · 2021 to 2025
$17.8M
Nano and biomolecular engineered technologies for neoantigen-specific T cell capture and characterizationR01CA264090 · NCI · INSTITUTE FOR SYSTEMS BIOLOGY · PI HEATH, JAMES R. · 2021 to 2025
$2.7M
NCATS NIH HHS UL1 TR001881NCI NIH HHS P30 CA015704NCI NIH HHS P50 CA097186NCI NIH HHS R01 CA264090NIAID NIH HHS P01 AI153559NIAID NIH HHS U19 AI057229
6 · The paper itself

Abstract

Antigen-specific T cell receptor (TCR) sequences can have prognostic, predictive, and therapeutic value, but decoding the specificity of TCR recognition remains challenging. Unlike DNA strands that base pair, TCRs bind to their targets with different orientations and different lengths, which complicates comparisons. We present scanning parametrized by normalized TCR length (SPAN-TCR) to analyze antigen-specific TCR CDR3 sequences and identify patterns driving TCR-pMHC specificity. Using entropic analysis, SPAN-TCR identifies 2-mer motifs that decrease the diversity (entropy) of CDR3s. These motifs are the most common patterns that can predict CDR3 composition, and we identify "essential" motifs that decrease entropy in the same CDR3 α or β chain containing the 2-mer, and "super-essential" motifs that decrease entropy in both chains. Molecular dynamics analysis further suggests that these motifs may play important roles in binding. We then employ SPAN-TCR to resolve similarities in TCR repertoires against different antigens using public databases of TCR sequences.

Indexed as

Receptors, Antigen, T-CellReceptors, Antigen, T-Cell, alpha-betaAmino Acid SequenceAntigensEntropyAntigensReceptors, Antigen, T-CellReceptors, Antigen, T-Cell, alpha-betaantigensCDR3 domainsSARS-COV-2T cell receptorsT cells

Identifiers

PMID37001518
PMCPMC10355346
OpenAlexW4361269528

What OpenQuestion holds

Textmetadata
LicenceTDM
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.