Format

Send to

Choose Destination
See comment in PubMed Commons below
Biochim Biophys Acta. 2011 Nov;1810(11):1025-34. doi: 10.1016/j.bbagen.2011.03.005. Epub 2011 Mar 21.

Epithelial, dendritic, and CD4(+) T cell regulation of and by reactive oxygen and nitrogen species in allergic sensitization.

Author information

1
Department of Chemistry, SUNY Plattsburgh, Plattsburgh, NY, United States.

Abstract

BACKGROUND:

While many of the contributing cell types and mediators of allergic asthma are known, less well understood are the factors that induce allergy in the first place. Amongst the mediators speculated to affect initial allergen sensitization and the development of pathogenic allergic responses to innocuous inhaled antigens and allergens are exogenously or endogenously generated reactive oxygen species (ROS) and reactive nitrogen species (RNS).

SCOPE OF REVIEW:

The interactions between ROS/RNS, dendritic cells (DCs), and CD4(+) T cells, as well as their modulation by lung epithelium, are of critical importance for the genesis of allergies that later manifest in allergic asthma. Therefore, this review will primarily focus on the initiation of pulmonary allergies and the role that ROS/RNS may play in the steps therein, using examples from our own work on the roles of NO(2) exposure and airway epithelial NF-κB activation.

MAJOR CONCLUSIONS:

Endogenously generated ROS/RNS and those encountered from environmental sources interact with epithelium, DCs, and CD4(+) T cells to orchestrate allergic sensitization through modulation of the activities of each of these cell types, which quantitiatively and qualitatively dictate the degree and type of the allergic asthma phenotype.

GENERAL SIGNIFICANCE:

Knowledge of the effects of ROS/RNS at the molecular and cellular levels has the potential to provide powerful insight into the balance between inhalational tolerance (the typical immunologic response to an innocuous inhaled antigen) and allergy, as well as to potentially provide mechanistic targets for the prevention and treatment of asthma.

PMID:
21397661
PMCID:
PMC3140554
DOI:
10.1016/j.bbagen.2011.03.005
[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science Icon for PubMed Central
    Loading ...
    Support Center