Evidence map›Paper›PMID 22547698›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2012

Delays and diversions mark the development of B cell responses to Borrelia burgdorferi infection.

Christine J Hastey, Rebecca A Elsner, Stephen W Barthold, Nicole Baumgarth

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

76 citing papers in PubMed, 99 citations in OpenAlex.

  1. Article
  2. Review
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  4. Review
  5. Seroprevalence ofPathogens (Basel, Switzerland) · 2026
    Observational
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  7. Article
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  11. Article
  12. Hitchhiker's Guide toJournal of bacteriology · 2024
    Review
  13. Article
  14. Suppression of host humoral immunity byInfection and immunity · 2024
    Article
  15. Article
  16. Concurrent Infection of the Human Brain with MultipleInternational journal of molecular sciences · 2023
    Article
  17. Article
  18. Antigen-Specific CD4 T Cell and B Cell Responses to Borrelia burgdorferi.Journal of immunology (Baltimore, Md. : 1950) · 2023
    Article
  19. Article
  20. Article

16 more citing papers are in PubMed but not listed here.

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 1 institution in 1 country.

Christine J HasteyGraduate Group in Microbiology, University of California, Davis, Davis, CA 95616, USA.
Rebecca A Elsner
Stephen W Barthold
Nicole Baumgarth
University of California, Davis · US

Funding

Animal Models of Infectious Diseases Training ProgramT32AI060555 · NIAID · UNIVERSITY OF CALIFORNIA DAVIS · PI MCSORLEY, STEPHEN J · 2004 to 2025
$3.3M
Humoral responses to Lyme Borreliosis: A mouse modelR01AI073911 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI BARTHOLD, STEPHEN WILLIAM, BAUMGARTH, NICOLE · 2008 to 2012
$1.9M
NIAID NIH HHS AI073911NIAID NIH HHS R01 AI073911NIAID NIH HHS T32 AI060555NIAID NIH HHS T32 AI060555
6 · The paper itself

Abstract

B cell responses modulate disease during infection with Borrelia burgdorferi, the causative agent of Lyme disease, but are unable to clear the infection. Previous studies have demonstrated that B. burgdorferi infection induces predominantly T-independent B cell responses, potentially explaining some of these findings. However, others have shown effects of T cells on the isotype profile and the magnitude of the B. burgdorferi-specific Abs. This study aimed to further investigate the humoral response to B. burgdorferi and its degree of T cell dependence, with the ultimate goal of elucidating the mechanisms underlying the failure of effective immunity to this emerging infectious disease agent. Our study identifies distinct stages in the B cell response using a mouse model, all marked by the generation of unusually strong and persistent T-dependent and T-independent IgM Abs. The initial phase is dominated by a strong T-independent accumulation of B cells in lymph nodes and the induction of specific Abs in the absence of germinal centers. A second phase begins around week 2.5 to 3, in which relatively short-lived germinal centers develop in lymph nodes, despite a lymph node architecture that lacks clearly demarcated T and B cell zones. This response failed, however, to generate appreciable numbers of long-lived bone marrow plasma cells. Finally, there is a slow accumulation of long-lived Ab-secreting plasma cells in bone marrow, reflected by a strong but ultimately ineffective serum Ab response. Overall, the study indicates that B. burgdorferi might evade B cell immunity by interfering with its response kinetics and quality.

Indexed as

AnimalsAntibodies, BacterialB-Lymphocyte SubsetsBorrelia burgdorferiCD40 AntigensCD4-Positive T-LymphocytesFemaleLyme DiseaseMaleMiceMice, 129 StrainMice, Inbred C57BLMice, KnockoutMice, SCIDTime FactorsAntibodies, BacterialCD40 Antigens

Identifiers

PMID22547698
PMCPMC3358496
OpenAlexW2169278706

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.