A Role for Regulatory T Cells in a Murine Model of Epicutaneous Toluene Diisocyanate Sensitization.

Toxicol Sci

*Allergy and Clinical Immunology Branch, Health Effects Laboratory Division, National Institute for Occupational Safety and Health, Centers for Disease Control and Prevention, Morgantown, West Virginia 26505.

Published: July 2016

Toluene diisocyanate (TDI) is a leading cause of chemical-induced occupational asthma which impacts workers in a variety of industries worldwide. Recently, the robust regulatory potential of regulatory T cells (Tregs) has become apparent, including their functional role in the regulation of allergic disease; however, their function in TDI-induced sensitization has not been explored. To elucidate the kinetics, phenotype, and function of Tregs during TDI sensitization, BALB/c mice were dermally exposed (on each ear) to a single application of TDI (0.5-4% v/v) or acetone vehicle and endpoints were evaluated via RT-PCR and flow cytometry. The draining lymph node (dLN) Treg population expanded significantly 4, 7, and 9 days after single 4% TDI exposure. This population was identified using a variety of surface and intracellular markers and was found to be phenotypically heterogeneous based on increased expression of markers including CD103, CCR6, CTLA4, ICOS, and Neuropilin-1 during TDI sensitization. Tregs isolated from TDI-sensitized mice were significantly more suppressive compared with their control counterparts, further supporting a functional role for Tregs during TDI sensitization. Last, Tregs were depleted prior to TDI sensitization and an intensified sensitization response was observed. Collectively, these data indicate that Tregs exhibit a functional role during TDI sensitization. Because the role of Tregs in TDI sensitization has not been previously elucidated, these data contribute to the understanding of the immunologic mechanisms of chemical induced allergic disease.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4987710PMC
http://dx.doi.org/10.1093/toxsci/kfw074DOI Listing

Publication Analysis

Top Keywords

tdi sensitization
24
functional role
12
tregs tdi
12
sensitization
9
tdi
9
regulatory cells
8
toluene diisocyanate
8
allergic disease
8
sensitization tregs
8
role tregs
8

Similar Publications

Targeting PGAM5 attenuates airway inflammation in asthma by inhibiting HMGB1 release in bronchial epithelial.

Free Radic Biol Med

January 2025

Chronic Airways Diseases Laboratory, Department of Respiratory and Critical Care Medicine, Nanfang Hospital, Southern Medical University, Guangzhou, 510515, China. Electronic address:

Article Synopsis
  • Previous studies linked high HMGB1 levels to the development of steroid-insensitive asthma caused by toluene diisocyanate (TDI), highlighting mitochondrial dysfunction in bronchial epithelia.
  • This study aims to determine if PGAM5, a mitochondrial protein, influences HMGB1 release in TDI-induced asthma by comparing its levels in asthma patients and healthy individuals and conducting various animal and in vitro experiments.
  • Findings showed that inhibiting PGAM5 reduced airway inflammation and HMGB1 release in TDI-exposed mice, illustrating a potential regulatory mechanism involving mitochondrial apoptosis-related processes.
View Article and Find Full Text PDF

Background: Isocyanates are used as starting materials of polyurethane (PU) products. They are relatively important occupational skin sensitizers.

Objectives: To analyse results of a large isocyanate patch test series of 19 isocyanate test substances and 4,4'-diaminodiphenylmethane (MDA), a marker of 4,4'-diphenylmethane diisocyanate (MDI) hypersensitivity.

View Article and Find Full Text PDF

GLUT1 mediates bronchial epithelial E-cadherin disruption in TDI-induced steroid-insensitive asthma.

J Asthma

November 2024

Department of Pulmonary and Critical Care Medicine, Zhujiang Hospital, Southern Medical University, Guangzhou, China.

Objective: Down-regulation of bronchial epithelial E-cadherin is an important of feature of severe asthma, including steroid-insensitive asthma. Yet, the mechanisms involved in E-cadherin disruption are not fully understood. This study was aimed to investigate the role of glucose transporter 1 (GLUT1) in dysregulation of E-cadherin in toluene diisocyanate (TDI)-induced steroid-insensitive asthma.

View Article and Find Full Text PDF

Background: Itch sensitization has been reported in patients with chronic allergic skin diseases and observed in a mouse model of allergic contact dermatitis (ACD). There is evidence suggesting that neuroimmune interactions may contribute to itch sensitization, as an increase in dendritic cells (DCs) within ganglia has been observed during allergic conditions. However, how DCs interact with sensory neurons in ganglia during allergic conditions is still not known.

View Article and Find Full Text PDF

Subanesthetic ketamine is increasingly used for the treatment of varied psychiatric conditions, both on- and off-label. While it is commonly classified as an N-methyl D-aspartate receptor (NMDAR) antagonist, our picture of ketamine's mechanistic underpinnings is incomplete. Recent clinical evidence has indicated, controversially, that a component of the efficacy of subanesthetic ketamine may be opioid dependent.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!