Evidence map›Paper›PMID 36639222›Full record

ArticleLife science alliance2023

Lineage tracing reveals fate bias and transcriptional memory in human B cells.

Michael Swift, Felix Horns, Stephen R Quake

Abstract read
In one paragraph

Article in Life science alliance, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Cell lineage tracing: Methods, applications, and challenges.Quantitative biology (Beijing, China) · 2025
    Review
  2. Long-term B cell memory emerges at uniform relative rates in the human immune response.Proceedings of the National Academy of Sciences of the United States of America · 2025
    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

3 authors.

Michael SwiftDepartment of Chemical and Systems Biology, Stanford University, Stanford, CA, USA michael.swift@stanford.edu steve@quake-lab.org.ORCID https://orcid.org/0000-0001-6391-0050
Felix HornsDivision of Biology and Bioengineering, California Institute of Technology, Pasadena, CA, USA.
Stephen R QuakeDepartment of Bioengineering, Stanford University, Stanford, CA, USA michael.swift@stanford.edu steve@quake-lab.org.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We combined single-cell transcriptomics and lineage tracing to understand fate choice in human B cells. Using the antibody sequences of B cells, we tracked clones during in vitro differentiation. Clonal analysis revealed a subset of IgM+ B cells which were more proliferative than other B-cell types. Whereas the population of B cells adopted diverse states during differentiation, clones had a restricted set of fates available to them; there were two times more single-fate clones than expected given population-level cell-type diversity. This implicated a molecular memory of initial cell states that was propagated through differentiation. We then identified the genes which had strongest coherence within clones. These genes significantly overlapped known B-cell fate determination programs, suggesting the genes which determine cell identity are most robustly controlled on a clonal level. Persistent clonal identities were also observed in human plasma cells from bone marrow, indicating that these transcriptional programs maintain long-term cell identities in vivo. Thus, we show how cell-intrinsic fate bias influences differentiation outcomes in vitro and in vivo.

Indexed as

B-LymphocytesImmunoglobulinsBone MarrowCell DifferentiationClone CellsHumansImmunoglobulins

Identifiers

PMID36639222
PMCPMC9840405

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Registered trials

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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.