Evidence map›Paper›PMID 27889108›Full record

ArticleImmunity2016

Positive Regulation of Lyn Kinase by CD148 Is Required for B Cell Receptor Signaling in B1 but Not B2 B Cells.

Katarzyna M Skrzypczynska, Jing W Zhu, Arthur Weiss

Open access · bronzeAbstract read
In one paragraph

Article in Immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
0.6field-weighted citation impact, top 29% 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

22 citing papers in PubMed, 38 citations in OpenAlex.

  1. Article
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  12. Immunoglobulin M-degrading enzyme ofFrontiers in immunology · 2023
    Article
  13. Review
  14. Article
  15. Review
  16. CD148 Deficiency in Fibroblasts Promotes the Development of Pulmonary Fibrosis.American journal of respiratory and critical care medicine · 2021
    Article
  17. Article
  18. Article
  19. B-1 cell responses to infections.Current opinion in immunology · 2019
    Review
  20. 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 at 1 institution in 1 country.

Katarzyna M SkrzypczynskaHoward Hughes Medical Institute, Rosalind Russell and Ephraim P. Engleman Rheumatology Research Center, Departments of Medicine and of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143-0795, USA.
Jing W ZhuHoward Hughes Medical Institute, Rosalind Russell and Ephraim P. Engleman Rheumatology Research Center, Departments of Medicine and of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143-0795, USA.
Arthur WeissHoward Hughes Medical Institute, Rosalind Russell and Ephraim P. Engleman Rheumatology Research Center, Departments of Medicine and of Microbiology and Immunology, University of California, San Francisco, San Francisco, CA 94143-0795, USA. Electronic address: art.weiss@ucsf.edu.
Howard Hughes Medical Institute · US

Funding

Microbial Pathogenesis and Host DefenseT32AI060537 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joanne N. Engel · 2004 to 2026
$6.5M
Howard Hughes Medical InstituteNIAID NIH HHS T32 AI060537
6 · The paper itself

Abstract

B1 and B2 B cells differ in their ability to respond to T-cell-independent (TI) antigens. Here we report that the Src-family kinase (SFK) regulator CD148 has a unique and critical role in the initiation of B1 but not B2 cell antigen receptor signaling. CD148 loss-of-function mice were found to have defective B1 B-cell-mediated antibody responses against the T-cell-independent antigens NP-ficoll and Pneumovax 23 and had impaired selection of the B1 B cell receptor (BCR) repertoire. These deficiencies were associated with a decreased ability of B1 B cells to induce BCR signaling downstream of the SFK Lyn. Notably, Lyn appeared to be selectively regulated by CD148 and loss of this SFK resulted in opposite signaling phenotypes in B1 and B2 B cells. These findings reveal that the function and regulation of Lyn during B1 cell BCR signaling is distinct from other B cell subsets.

Indexed as

AnimalsB-Lymphocyte SubsetsEnzyme-Linked Immunosorbent AssayEnzyme-Linked Immunospot AssayFlow CytometryLymphocyte ActivationMiceMice, KnockoutReceptor-Like Protein Tyrosine Phosphatases, Class 3Receptors, Antigen, B-CellSignal Transductionsrc-Family Kinaseslyn protein-tyrosine kinasePtprj protein, mouseReceptor-Like Protein Tyrosine Phosphatases, Class 3Receptors, Antigen, B-Cellsrc-Family KinasesB1 B cellBCRCD148DEP-1LynPneumovax 23PtprjT-cell-independent

Identifiers

PMID27889108
PMCPMC5903562
OpenAlexW2552997261

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.