Evidence map›Paper›PMID 24978161›Full record

ArticleNature communications2014

Shp1 signalling is required to establish the long-lived bone marrow plasma cell pool.

Yan-Feng Li, Shengli Xu, Xijun Ou, Kong-Peng Lam

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.4field-weighted citation impact, top 19% 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

19 citing papers in PubMed, 33 citations in OpenAlex.

  1. B cell receptor ligation induces IgE plasma cell elimination.The Journal of experimental medicine · 2023
    Article
  2. Article
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  6. Article
  7. Review
  8. Two DuplicatedFrontiers in immunology · 2021
    Article
  9. Article
  10. Article
  11. A signalling cascade involving receptor-activated phospholipase ACell communication and signaling : CCS · 2019
    Article
  12. Review
  13. Cochaperone Mzb1 is a key effector of Blimp1 in plasma cell differentiation and β1-integrin function.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
  14. Review
  15. Shp1 function in myeloid cells.Journal of leukocyte biology · 2017
    Review
  16. Article
  17. Article
  18. Article
  19. 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

4 authors at 3 institutions in 1 country.

Yan-Feng LiImmunology Group, Bioprocessing Technology Institute, Agency for Science, Technology and Research, Singapore 138668, Singapore.
Shengli Xu1] Immunology Group, Bioprocessing Technology Institute, Agency for Science, Technology and Research, Singapore 138668, Singapore [2] Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore.
Xijun OuImmunology Group, Bioprocessing Technology Institute, Agency for Science, Technology and Research, Singapore 138668, Singapore.
Kong-Peng Lam1] Immunology Group, Bioprocessing Technology Institute, Agency for Science, Technology and Research, Singapore 138668, Singapore [2] Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore [3] Department of Microbiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore [4] Department of Pediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Singapore 117599, Singapore.
Bioprocessing Technology Institute · SGAgency for Science, Technology and Research · SGNational University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Germline or B-cell-specific loss of Ptpn6 gene encoding the Shp1 protein tyrosine phosphatase leads to skewed B lymphopoiesis and systemic autoimmunity. Here, to study its role in B-cell terminal differentiation, we generated Ptpn6(f/f)Aicda(Cre/+) mice with Shp1 ablated only in activated B cells. We show that Ptpn6(f/f)Aicda(Cre/+) mice have normal B-cell development but exhibit defective class-switched primary and recalled antibody response to a T-cell-dependent antigen. Germinal centres are present but do not persist and memory B cells are not formed. Interestingly, Shp1-deficient plasma cells are generated in the spleen but do not contribute to the bone marrow long-lived pool. Plasma cells lacking Shp1 exhibit aberrant α4β1 integrin activation due to dysregulated Src- and PI3-kinase signalling and manifest attenuated migration in vitro and defective bone marrow homing when reconstituted in vivo. Interrupting α4β1-VCAM-1 interaction rectifies this defect. These data suggest that Shp1 signalling is required for the establishment of a life-long protective humoral immunity.

Indexed as

AICDA (Activation-Induced Cytidine Deaminase)AnimalsB-LymphocytesBone MarrowCell DifferentiationCytidine DeaminaseFemaleMaleMicePhosphatidylinositol 3-KinasesPlasma CellsProtein Tyrosine Phosphatase, Non-Receptor Type 6Signal TransductionT-LymphocytesAICDA (Activation-Induced Cytidine Deaminase)Cytidine DeaminasePhosphatidylinositol 3-KinasesProtein Tyrosine Phosphatase, Non-Receptor Type 6Ptpn6 protein, mouse

Identifiers

PMID24978161
PMCPMC4083441
OpenAlexW2171080996

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.