Evidence map›Paper›PMID 15774582›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Defective B cell responses in the absence of SH2D1A.

Massimo Morra, Robert A Barrington, Ana C Abadia-Molina, Susumo Okamoto, Aimee Julien, Charles Gullo, Anuj Kalsy, Matthew J Edwards, Gang Chen, Rosanne Spolski and 7 more

Open access · greenAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

29 citing papers in PubMed, 73 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Genes known to escape X chromosome inactivation predict co-morbid chronic musculoskeletal pain and posttraumatic stress symptom development in women following trauma exposure.American journal of medical genetics. Part B, Neuropsychiatric genetics : the official publication of the International Society of Psychiatric Genetics · 2019
    Article
  6. Review
  7. Review
  8. Article
  9. SAP and Lessons Learned from a Primary Immunodeficiency.Journal of immunology (Baltimore, Md. : 1950) · 2017
    Article
  10. Article
  11. Review
  12. Staphylococcal Enterotoxin B (SEB) Induces Memory CD4 T Cell AnergyJournal of clinical & cellular immunology · 2015
    Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
  19. Article
  20. Follicular helper T cells are required for systemic autoimmunity.The Journal of experimental medicine · 2009
    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

17 authors at 3 institutions in 1 country.

Massimo MorraDivision of Immunology, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 02215, USA. mmorra@bidmc.harvard.edu
Robert A Barrington
Ana C Abadia-Molina
Susumo Okamoto
Aimee Julien
Charles Gullo
Anuj Kalsy
Matthew J Edwards
Gang Chen
Rosanne Spolski
Warren J Leonard
Brigitte T Huber
Persephone Borrow
Christine A Biron
Abhay R Satoskar
Michael C Carroll
Cox Terhorst
Brown University · USThe Ohio State University · USTufts University · US

Funding

TRANSGENIC MODELS OF T CELL RECEPTOR IMMUNODEFICIENCIESP01AI035714 · NIAID · BETH ISRAEL DEACONESS MEDICAL CENTER · PI TERHORST, CORNELIS P · 1994 to 2007
$9.3M
NIAID NIH HHS AI-35714NIAID NIH HHS P01 AI035714
6 · The paper itself

Abstract

More than half of patients with X-linked lympho-proliferative disease, which is caused by a defect in the intracellular adapter protein SH2D1A, suffer from an extreme susceptibility to Epstein-Barr virus. One-third of these patients, however, develop dysgammaglobulenemia without an episode of severe mononucleosis. Here we show that in SH2D1A(-/-) mice, both primary and secondary responses of all Ig subclasses are severely impaired in response to specific antigens. Because germinal centers were absent in SH2D1A(-/-) mice upon primary immunization, and because SH2D1A was detectable in wt germinal center B cells, we examined whether SH2D1A(-/-) B cell functions were impaired. Using the adoptive cotransfer of B lymphocytes from hapten-primed SH2D1A(-/-) mice with CD4(+) T cells from primed wt mice into irradiated wt mice provided evidence that signal transduction events controlled by SH2D1A are essential for B cell activities resulting in antigen specific IgG production. Defects in naive SH2D1A(-/-) B cells became evident upon cotransfer with non-primed wt CD4(+) cells into Rag2(-/-) recipients. Thus, both defective T and B cells exist in the absence of SH2D1A, which may explain the progressive dysgammaglobulinemia in a subset of X-linked lympho-proliferative disease patients without involvement of Epstein-Barr virus.

Indexed as

Adoptive TransferAnimalsB-LymphocytesDysgammaglobulinemiaEnzyme-Linked Immunosorbent AssayFlow CytometryFluorescent Antibody TechniqueHaptensHemocyaninsHistological TechniquesImmunoglobulin GIntracellular Signaling Peptides and ProteinsLymphocytic choriomeningitis virusLymphoproliferative DisordersMiceMice, Inbred Strains4-hydroxy-3-nitrophenylacetyl-keyhole limpet hemocyaninHaptensHemocyaninsImmunoglobulin GIntracellular Signaling Peptides and ProteinsSh2d1a protein, mouseSignaling Lymphocytic Activation Molecule Associated Protein

Identifiers

PMID15774582
PMCPMC555707
OpenAlexW2076124836

What OpenQuestion holds

Textmetadata
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.