Evidence map›Paper›PMID 20371392›Full record

ReviewThe Journal of allergy and clinical immunology2010

Clinical consequences of defects in B-cell development.

Andre M Vale, Harry W Schroeder

Abstract readReview
In one paragraph

Review in The Journal of allergy and clinical immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

44 citing papers in PubMed, 94 citations in OpenAlex.

  1. Trial
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Review
  19. Article
  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

2 authors at 1 institution in 1 country.

Andre M ValeDivision of Clinical Immunology and Rheumatology, Department of Medicine, University of Alabama at Birmingham, Birmingham, Ala, USA.
Harry W Schroeder
University of Alabama at Birmingham · US

Funding

The role of Immunoglobulin CDRH3 in Autoimmune DiseaseR01AI048115 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SCHROEDER, HARRY WILLIAM · 2000 to 2010
$3.1M
HLA Region and KIR Genomics in Common Variable Immune DeficiencyU01AI090902 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SCHROEDER, HARRY WILLIAM · 2010 to 2014
$2.9M
Role of IG CDR-H3 in Responses to HIV VaccinesR01AI090742 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SCHROEDER, HARRY WILLIAM · 2010 to 2013
$1.5M
HLA*B Associated Genes and Memory B cells in patients with CVIDR21AI079741 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SCHROEDER, HARRY WILLIAM · 2008 to 2009
$571k
Immunoglobulin CDR-H3 and neutralizing antibodies to HIVR21AI078449 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SCHROEDER, HARRY WILLIAM · 2008 to 2009
$510k
Role of immunoglobulin CDR-H3 in heterosubtypic immunity to influenza virusR21AI088498 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SCHROEDER, HARRY WILLIAM · 2010 to 2011
$401k
The Role of Immunoglobulin CDRH3 in Autoimmune DiseaseR56AI048115 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI SCHROEDER, HARRY WILLIAM · 2012 to 2012
$366k
NIAID NIH HHS AI078449NIAID NIH HHS AI079741NIAID NIH HHS AI48115,NIAID NIH HHS R01 AI048115NIAID NIH HHS R01 AI090742NIAID NIH HHS R21 AI078449NIAID NIH HHS R21 AI079741NIAID NIH HHS R21 AI088498NIAID NIH HHS R56 AI048115NIAID NIH HHS U01 AI090902
6 · The paper itself

Abstract

Abnormalities in humoral immunity typically reflect a generalized or selective failure of effective B-cell development. The developmental processes can be followed through analysis of cell-surface markers, such as IgM, IgD, CD10, CD19, CD20, CD21, and CD38. Early phases of B-cell development are devoted to the creation of immunoglobulin and testing of B-cell antigen receptor signaling. Failure leads to the absence of B cells and immunoglobulin in the blood from birth. As the developing B cells begin to express a surface B-cell receptor, they become subject to negative and positive selection pressures and increasingly depend on survival signals. Defective signaling can lead to selective or generalized hypogammaglobulinemia, even in the presence of normal numbers of B cells. In the secondary lymphoid organs some B cells enter the splenic marginal zone, where preactivated cells lie ready to rapidly respond to T-independent antigens, such as the polysaccharides that coat some microorganisms. Other cells enter the follicle and, with the aid of cognate follicular T cells, divide to help form a germinal center (GC) after their interaction with antigen. In the GC B cells can undergo the processes of class switching and somatic hypermutation. Failure to properly receive T-cell signals can lead to hyper-IgM syndrome. B cells that leave the GC can develop into memory B cells, short-lived plasma cells, or long-lived plasma cells. The latter ultimately migrate back to the bone marrow, where they can continue to produce protective antigen-specific antibodies for decades.

Indexed as

B-LymphocytesCell DifferentiationCommon Variable ImmunodeficiencyHumansImmunity, HumoralImmunologic Memory

Identifiers

PMID20371392
PMCPMC3653433
OpenAlexW2151424860

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.