Evidence map›Paper›PMID 28049042›Full record

ArticleToxicology2017

Aryl hydrocarbon receptor activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin impairs human B lymphopoiesis.

Jinpeng Li, Ashwini S Phadnis-Moghe, Robert B Crawford, Norbert E Kaminski

Abstract read
In one paragraph

Article in Toxicology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.9field-weighted citation impact, top 17% 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

17 citing papers in PubMed, 27 citations in OpenAlex.

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  12. Effects of environmental stressors on stem cells.World journal of stem cells · 2019
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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

4 authors at 1 institution in 1 country.

Jinpeng LiGenetics Program, Michigan State University, East Lansing, MI, 48824, United States; Institute for Integrative Toxicology, Michigan State University, East Lansing, MI, 48824, United States.
Ashwini S Phadnis-MogheInstitute for Integrative Toxicology, Michigan State University, East Lansing, MI, 48824, United States.
Robert B CrawfordInstitute for Integrative Toxicology, Michigan State University, East Lansing, MI, 48824, United States; Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, 48824, United States.
Norbert E KaminskiInstitute for Integrative Toxicology, Michigan State University, East Lansing, MI, 48824, United States; Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI, 48824, United States. Electronic address: kamins11@msu.edu.
Michigan State University · US

Funding

TOXIC EFFECTS OF TCDD ON B CELLSR01ES002520 · NIEHS · VIRGINIA COMMONWEALTH UNIVERSITY · PI KAMINSKI, NORBERT E · 1986 to 2016
$4.2M
NIEHS NIH HHS R01 ES002520
6 · The paper itself

Abstract

The homeostasis of peripheral B cell compartment requires lifelong B lymphopoiesis from hematopoietic stem cells (HSC). As a result, the B cell repertoire is susceptible to disruptions of hematopoiesis. Increasing evidence, primarily from rodent models, shows that the aryl hydrocarbon receptor (AHR) regulates hematopoiesis. To study the effects of persistent AHR activation on human B cell development, a potent AHR agonist and known environmental contaminant, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) was utilized. An in vitro B cell development model system was established by co-culturing human cord blood-derived HSCs with irradiated human primary bone marrow stromal cells. Using this in vitro model, we found that TCDD significantly suppressed the total number of hematopoietic stem and progenitor cells (HSPC) in a concentration-dependent manner. Cell death analysis demonstrated that the decrease in cell number was not due to cytotoxicity by TCDD. In addition, TCDD markedly decreased CD34 expression on HSPCs. Structure-activity relationship studies using dioxin congeners demonstrated a correlation between the relative AHR binding affinity and the magnitude of decrease in the number of HSPCs and CD34 expression, suggesting that AHR mediates the observed TCDD-elicited changes in HSPCs. Moreover, a significant reduction in lineage committed B cell-derived from HSCs was observed in the presence of TCDD, indicating impairment of human B cell development. Similar effects of TCDD were observed regardless of the use of stromal cells in cultures indicating a direct effect of TCDD on HSCs. Collectively, we demonstrate that AHR activation by TCDD on human HSCs impairs early stages of human B lymphopoiesis.

Indexed as

B-LymphocytesCells, CulturedCoculture TechniquesEnvironmental PollutantsHematopoietic Stem CellsHumansLymphopoiesisPolychlorinated DibenzodioxinsReceptors, Aryl HydrocarbonEnvironmental PollutantsPolychlorinated DibenzodioxinsReceptors, Aryl Hydrocarbon2,3,7,8-Tetrachlorodibenzo-p-dioxinAryl hydrocarbon receptorHematopoietic stem cellHuman B lymphopoiesis

Identifiers

PMID28049042
PMCPMC5293665
OpenAlexW2564875073

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.