Evidence map›Paper›PMID 15972507›Full record

ArticleInfection and immunity2005

Neisseria gonorrhoeae kills carcinoembryonic antigen-related cellular adhesion molecule 1 (CD66a)-expressing human B cells and inhibits antibody production.

Milica Pantelic, Young-June Kim, Silvia Bolland, Ines Chen, John Shively, Tie Chen

Open access · greenAbstract read
In one paragraph

Article in Infection and immunity, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.8field-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

47 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Diversity and evolution of a phase-variable multi-locus antigen inbioRxiv : the preprint server for biology · 2026
    Article
  3. Article
  4. Article
  5. Experimental Urethral Infection with Neisseria gonorrhoeae.Current topics in microbiology and immunology · 2024
    Review
  6. Review
  7. Mechanisms of host manipulation byFrontiers in microbiology · 2023
    Review
  8. Tissue Models forFrontiers in cellular and infection microbiology · 2022
    Review
  9. Review
  10. Article
  11. Article
  12. Article
  13. Journal of cell death · 2018
    Article
  14. Article
  15. Gonorrhea - an evolving disease of the new millennium.Microbial cell (Graz, Austria) · 2016
    Review
  16. Article
  17. Article
  18. Article
  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

6 authors at 4 institutions in 1 country.

Milica PantelicDepartment of Microbiology and Immunology, Division of Infectious Diseases, Walther Oncology Center, Indiana University School of Medicine, MS415E, 635 Barnhill Dr., Indianapolis, Indiana 46202-5120, USA.
Young-June Kim
Silvia Bolland
Ines Chen
John Shively
Tie Chen
Indiana University – Purdue University Indianapolis · USCity of Hope · USIndiana University School of MedicineNational Institute of Allergy and Infectious Diseases · US

Funding

Regulation Of The Immune Response By The Inositol Phosphatase SHIPZ01AI000911 · NIAID · NIAID EXTRAMURAL ACTIVITIES · PI BOLLAND, SILVIA · 2002 to 2008
$1.3M
ROLES OF CD66 ANTIGENS IN INFECTION BY N GONORRHOEAER01AI047736 · NIAID · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI CHEN, TIE · 1999 to 2003
$668k
Mechanisms of Host Responses in GonorrheaR03TW006270 · FIC · UNIVERSITY OF ILLINOIS AT CHICAGO · PI CHEN, TIE · 2004 to 2006
$107k
FIC NIH HHS R03 TW006270FIC NIH HHS R03TW006270NIAID NIH HHS R01 AI047736PHS HHS R01A1 47736
6 · The paper itself

Abstract

Neisseria gonorrhoeae cells (gonococci [GC]), the etiological agents for gonorrhea, can cause repeated infections. During and after gonococcal infection, local and systemic antigonococcal antibody levels are low. These clinical data indicate the possibility that GC may suppress immune responses during infection. Carcinoembryonic antigen-related cellular adhesion molecule 1 (CEACAM1 or CD66a), a receptor for GC opacity (Opa) proteins, was shown to mediate inhibitory signals. In the present study, human B cells were activated by interleukin-2 to express CEACAM1 and then stimulated to secrete antibodies and simultaneously coincubated with Opa- and OpaI GC of strain MS11. Our results show that this OpaI GC has the ability to inhibit antibody production. The interaction of GC and CEACAM1 with human peripheral B cells also results in induction of cell death. The same findings were observed in DT40 B cells. This CEACAM1-promoted cell death pathway does not involve the inhibitory signals or the tyrosine phosphatases SHP-1 and SHP-2 but depends on Bruton's tyrosine kinase in DT40 cells. Our results suggest that Neisseria gonorrhoeae possesses the ability to suppress antibody production by killing CEACAM1-expressing B cells.

Indexed as

Antibody FormationImmune ToleranceAgammaglobulinaemia Tyrosine KinaseAnimalsAntigens, CDAntigens, DifferentiationApoptosisBacterial Outer Membrane ProteinsB-LymphocytesCell Adhesion MoleculesCell DeathCell LineChickensEnzyme PrecursorsHumansInterleukin-2Agammaglobulinaemia Tyrosine KinaseAntigens, CDAntigens, DifferentiationBacterial Outer Membrane ProteinsCD66 antigensCell Adhesion MoleculesEnzyme PrecursorsInterleukin-2Intracellular Signaling Peptides and ProteinsOpa protein, NeisseriaProtein-Tyrosine KinasesSyk KinaseSYK protein, human

Identifiers

PMID15972507
PMCPMC1168567
OpenAlexW2150608326

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.