Evidence map›Paper›PMID 15845474›Full record

ArticleInfection and immunity2005

Differential binding of Escherichia coli enterotoxins LT-IIa and LT-IIb and of cholera toxin elicits differences in apoptosis, proliferation, and activation of lymphoid cells.

Sergio Arce, Hesham F Nawar, Michael W Russell, Terry D Connell

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 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.6field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 39 citations in OpenAlex.

  1. Review
  2. Recent advances in respiratory immunization: A focus on COVID-19 vaccines.Journal of controlled release : official journal of the Controlled Release Society · 2023
    Review
  3. Oral exposure toFrontiers in immunology · 2023
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
  10. Glycosphingolipid functions.Cold Spring Harbor perspectives in biology · 2011
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Review
  19. Review
  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

4 authors at 1 institution in 1 country.

Sergio ArceDepartment of Microbiology and Immunology, The University of Buffalo, State University of New York at Buffalo, 138 Farber Hall, 3435 Main St., Buffalo, NY 12214, USA. arce@buffalo.edu
Hesham F Nawar
Michael W Russell
Terry D Connell
University at Buffalo, State University of New York · US

Funding

TYPE II Enterotoxins as Mucosal ImmunomodulatorsR01DE013833 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI CONNELL, TERRY D. · 2001 to 2010
$3.2M
ANTIGENS OF STREPTOCOCCUS MUTANS IN CARIES IMMUNITYR37DE006746 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RUSSELL, MICHAEL W · 1999 to 2008
$2.4M
Mechanisms of Adjuvant StimulationK02DE014357 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI CONNELL, TERRY D. · 2002 to 2006
$526k
Type II enterotoxins as mucosal immunomodulatorsR56DE013833 · NIDCR · STATE UNIVERSITY OF NEW YORK AT BUFFALO · PI CONNELL, TERRY D. · 2011 to 2011
$317k
PROTEIN ANTIGENS OF STREP MUTANS IN CARIES IMMUNITYR01DE006746 · NIDCR · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI RUSSELL, MICHAEL W · 1985 to 1998
–
NIDCR NIH HHS DE014357NIDCR NIH HHS DE06746NIDCR NIH HHS DE13833NIDCR NIH HHS K02 DE014357NIDCR NIH HHS R01 DE013833NIDCR NIH HHS R37 DE006746NIDCR NIH HHS R56 DE013833
6 · The paper itself

Abstract

Cholera toxin (CT), LT-IIa, and LT-IIb are potent adjuvants which induce distinct T-helper (Th)-cell cytokine profiles and immunoglobulin G (IgG) subclass and IgA antibody responses. To determine if the distinct immune regulatory effects observed for LT-IIa, LT-IIb, and CT are elicited by binding of the enterotoxins to their cognate ganglioside receptors, the lineages of lymphoid cells that interact with the three enterotoxins and their effects on various lymphocyte responses in vitro were evaluated. Binding patterns of LT-IIa, LT-IIb, and CT to several lymphoid cell populations were distinctive for each enterotoxin. LT-IIa and CT, but not LT-IIb, induced apoptosis in CD8(+) T cells. LT-IIa(T34I), a mutant with no detectable binding to gangliosides, did not induce apoptosis. Blockade of GM(1) on the surface of CD8(+) T cells by LT-IIa(T14I), a mutant that binds only to GM(1) but does not induce apoptosis, did not inhibit induction of apoptosis by LT-IIa. Mitogen-induced proliferation of CD8(+) T cells was abrogated by treatment with CT, while resting CD8(+) T cells which were sensitive to LT-IIa-induced apoptosis became more resistant to apoptosis after mitogen activation. Exposure to CT, but not to LT-IIa or LT-IIb, inhibited mitogen-driven CD4(+) T-cell proliferation and expression of CD25 and CD69. In mitogen-stimulated B cells, CT, but not LT-IIa or LT-IIb, enhanced expression levels of CD86, while only CT induced B-cell differentiation into plasma cells. Thus, LT-IIa, LT-IIb, and CT exhibit distinguishable immunomodulatory properties which are likely dependent upon their capacities to recognize different ganglioside receptors on lymphocytes.

Indexed as

ApoptosisAnimalsBacterial ToxinsB-LymphocytesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCholera ToxinEnterotoxinsEscherichia coliEscherichia coli ProteinsFemaleLymphocyte ActivationLymphocytesMiceMice, Inbred BALB CReceptors, Cell SurfaceBacterial ToxinsCholera ToxinEnterotoxinsEscherichia coli Proteinsganglioside receptorheat-labile enterotoxin, E coliReceptors, Cell Surface

Identifiers

PMID15845474
PMCPMC1087339
OpenAlexW2170464539

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.