TREM-2 and Dendritic Cells in the Pathogenesis of Allergic Airway Inflammation
type: CreativeWork
description: Asthma is a chronic disorder of the conducting airways that involves the interplay of multiple genetic and environmental factors. It is characterized by reversible airway obstruction, cellular infiltration, airway inflammation and airway remodeling. Dendritic cells (DCs) are professional antigen presenting cells that initiate the asthmatic inflammatory response by capturing inhaled antigens and migrating to the lymph nodes to mediate T-helper cell responses. Lung DCs consist of a heterogenous population of cells that express CD11c and are further divided into two major subsets based on the expression of CD11b and CD103. Both subsets have been shown to drive pro- or anti-inflammatory responses based on stimulus and cytokine environment.|Dendritic cells express several pattern recognition receptors (PRRs) that are critical for their function as sentinels of the immune system. DC maturation can be induced by several signaling pathways, such as TLR, Fc receptors and DAP-12 mediated -signaling, based on the activating signal. The recently discovered triggering receptor expressed on myeloid cells (TREM)-2 belongs to a family of cell surface receptors that mediate signaling via associations with the DAP-12 adaptor protein. TREM-2 is expressed on DCs, microglia and macrophages and was originally described as an anti-inflammatory mediator. However, recent studies have shown that the TREM-2/DAP-12 pathway can provide both anti-inflammatory and pro-inflammatory signals based on the micro-environment. Although TREM-2 has been shown to play a role in several inflammatory diseases, its expression in the airways and role in allergic airway inflammation is yet to be elucidated. Given that TREM-2 has been shown to drive inflammation in other disease models, we hypothesized that TREM-2 might play a role in the onset and progression of allergic airway inflammation.|Sensitization and challenge with ovalbumin was shown to reproduce hallmark features of allergic airway inflammation. Anal…
abstract: Asthma is a chronic disorder of the conducting airways that involves the interplay of multiple genetic and environmental factors. It is characterized by reversible airway obstruction, cellular infiltration, airway inflammation and airway remodeling. Dendritic cells (DCs) are professional antigen presenting cells that initiate the asthmatic inflammatory response by capturing inhaled antigens and migrating to the lymph nodes to mediate T-helper cell responses. Lung DCs consist of a heterogenous population of cells that express CD11c and are further divided into two major subsets based on the expression of CD11b and CD103. Both subsets have been shown to drive pro- or anti-inflammatory responses based on stimulus and cytokine environment.|Dendritic cells express several pattern recognition receptors (PRRs) that are critical for their function as sentinels of the immune system. DC maturation can be induced by several signaling pathways, such as TLR, Fc receptors and DAP-12 mediated -signaling, based on the activating signal. The recently discovered triggering receptor expressed on myeloid cells (TREM)-2 belongs to a family of cell surface receptors that mediate signaling via associations with the DAP-12 adaptor protein. TREM-2 is expressed on DCs, microglia and macrophages and was originally described as an anti-inflammatory mediator. However, recent studies have shown that the TREM-2/DAP-12 pathway can provide both anti-inflammatory and pro-inflammatory signals based on the micro-environment. Although TREM-2 has been shown to play a role in several inflammatory diseases, its expression in the airways and role in allergic airway inflammation is yet to be elucidated. Given that TREM-2 has been shown to drive inflammation in other disease models, we hypothesized that TREM-2 might play a role in the onset and progression of allergic airway inflammation.|Sensitization and challenge with ovalbumin was shown to reproduce hallmark features of allergic airway inflammation. Anal…
author: Hall, Sannette C.
language: en_US
date published: 2018-05-15
date modified: 2026-07-24T01:49:51Z
provider: Creighton University
publisher: Networked Digital Library of Theses and Dissertations
type: WebPage
source organization: Creighton University

PropertyValue
property ID: Handle
value: http://hdl.handle.net/10504/117934