Correlation of AHR Activation-Induced Suppression of PWM-Stimulated IgG and IgG-Triggered Signaling in Human PBMCs.

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In one paragraph

Article in Antibodies (Basel, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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1 · What the graph read from it

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Arpita DebCenter for Environmental Health Sciences and Department of Comparative Biomedical Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762, USA.ORCID 0009-0003-6685-0358

Barbara L F KaplanCenter for Environmental Health Sciences and Department of Comparative Biomedical Sciences, College of Veterinary Medicine, Mississippi State University, Mississippi State, MS 39762, USA.ORCID 0000-0002-1992-4145

Funding

TCDD-treated B Cells Modulate T Effector and T Regulatory Function in EAER15ES027650 · NIEHS · MISSISSIPPI STATE UNIVERSITY · PI KAPLAN, BARBARA LEE-FAUBERT · 2017 to 2022

$856k

NIEHS NIH HHS R15 ES027650NIH HHS 2R15ES027650-04

6 · The paper itself

Abstract

BACKGROUND/

objectivesAryl hydrocarbon receptor (AHR) ligands are known to suppress antibody production. However, it remains unclear whether this suppression translates into altered antibody-mediated Fcγ receptor signaling in human cells. This study aimed to investigate the effects and mechanisms by which AHR ligands regulate antibody production and antibody-triggered responses in human peripheral blood mononuclear cells (PBMCs).

methodsPBMCs were isolated from blood obtained from anonymous healthy donors. PBMCs were stimulated with pokeweed mitogen (PWM) to induce IgG1 production or Strept-Biotin IgG1/IgG2 immune complexes to induce antibody-triggered signaling. Before any stimulation, cells were pretreated with vehicle (0.01% DMSO) or AHR ligands TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin), ITE (2-(1H-indol-3-ylcarbonyl)-4-thiazolecarboxylic acid methyl ester), or FICZ (6-formylindolo[3,2-b]carbazole), or the proligand I3C (indole-3-carbinol).

resultsOur data revealed that PWM stimulation significantly increased

conclusionsOverall, these findings demonstrate that AHR activation by TCDD suppressed antibody production and IgG-mediated immune signaling in human PBMCs.

Indexed as

aryl hydrocarbon receptor (AHR)IgGindole-3-carbinol (I3C)

Identifiers

PMID42645425

DOI10.3390/antib15040068

PMCPMC13509459

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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.