Evidence map›Paper›PMID 20952503›Full record

ReviewToxicological sciences : an official journal of the Society of Toxicology2011

The long winding road toward understanding the molecular mechanisms for B-cell suppression by 2,3,7,8-tetrachlorodibenzo-p-dioxin.

Courtney E W Sulentic, Norbert E Kaminski

Open access · bronzeAbstract readReview
In one paragraph

Review in Toxicological sciences : an official journal of the Society of Toxicology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.5field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

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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 2 institutions in 1 country.

Courtney E W SulenticDepartment of Pharmacology & Toxicology, Boonshoft School of Medicine, Wright State University, Dayton, Ohio 45435, USA.
Norbert E Kaminski
Michigan State University · USWright State University · US

Funding

VOLATILE ORGANIC CONTAMINANTS--QUANTIFYING THEIR MOVEMENT IN THE UNSATURATED ZONEP42ES004911 · NIEHS · MICHIGAN STATE UNIVERSITY · PI Timothy R. Zacharewski · 1989 to 2026
$64.9M
TOXIC EFFECTS OF TCDD ON B CELLSR01ES002520 · NIEHS · VIRGINIA COMMONWEALTH UNIVERSITY · PI KAMINSKI, NORBERT E · 1986 to 2016
$4.2M
3'alpha enhancer regulation by AhR and NF-kappaB/Rel proteinsR01ES014676 · NIEHS · WRIGHT STATE UNIVERSITY · PI SULENTIC, COURTNEY ELIZABETH WILLIAMS · 2007 to 2011
$1.4M
NIEHS NIH HHS P42 ES004911NIEHS NIH HHS R01 ES002520NIEHS NIH HHS R01 ES014676NIEHS NIH HHS R01ES014676
6 · The paper itself

Abstract

Suppression of humoral immune responses by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was first reported in the mid-1970s. Since this initial observation, much effort has been devoted by many laboratories toward elucidation of the cellular and molecular mechanisms responsible for the profound impairment of humoral immune responses by TCDD, which is characterized by decreased B cell to plasma cell differentiation and suppression of immunoglobulin production. These efforts have led to a significant body of research demonstrating a direct effect of TCDD on B-cell maturation and function as well as a requisite but as yet undefined role of the aryl hydrocarbon receptor (AhR) in these effects. Likewise, a number of molecular targets putatively involved in mediating B-cell dysfunction by TCDD, and other AhR ligands, have been identified. However, our current understanding has primarily relied on findings from mouse models, and the translation of this knowledge to effects on human B cells and humoral immunity in humans is less clear. Therefore, a current challenge is to determine how TCDD and the AhR affect human B cells. Efforts have been made in this direction but continued progress in developing adequate human models is needed. An in-depth discussion of these advances and limitations in elucidating the cellular and molecular mechanisms putatively involved in the suppression of B-cell function by TCDD as well as the implications on human diseases associated in epidemiological studies with exposure to TCDD and dioxin-like compounds is the primary focus of this review.

Indexed as

AnimalsB-LymphocytesCells, CulturedEnvironmental PollutantsGene Expression RegulationHumansImmunity, HumoralImmunomodulationMicePolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonEnvironmental PollutantsPolychlorinated DibenzodioxinsReceptors, Aryl Hydrocarbon

Identifiers

PMID20952503
PMCPMC3043085
OpenAlexW2136524980

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.