Myeloid dendritic cells induce Th2 responses to inhaled antigen, leading to eosinophilic airway inflammation

Lambrecht, Bart N.; Veerman, Marijke de; Coyle, Anthony J.; Gutierrez-Ramos, José-Carlos; Thielemans, Kris; Pauwels, Romain

doi:10.1172/jci8107

Cited by 467 publications

(472 citation statements)

References 42 publications

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“…Early recruitment of antigen-presenting cells into the airways, an important element of the initial inflammatory response, 24,49 paralleled release of TNF-α, with a peak 1 hour after allergen challenge of sensitized mice. On the other hand, appearance of high levels of SP-D 48 hours later coincided with a second wave of mononuclear cell influx but no TNF-α release.…”

Section: Discussionmentioning

confidence: 99%

“…Plasmacytoid dendritic cells make up the majority under baseline conditions, 23 and these cells were shown to be tolerogenic in allergen-induced inflammation. [24][25][26] On the other hand, myeloid dendritic cells migrate rapidly to the lung during T H 2-type inflammation and exert potent T H 2 cell activation. [24][25][26] Dendritic cells are generally differentiated by the membrane marker CD11c, although this marker is shared with alveolar macrophages.…”

Section: Tnf; Sp-d; Dendritic Cell; Mouse Model; Airway Inflammationmentioning

confidence: 99%

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Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

Hortobagyi

Kierstein

Krytska

et al. 2008

Journal of Allergy and Clinical Immunology

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Section: Discussionmentioning

confidence: 99%

Section: Tnf; Sp-d; Dendritic Cell; Mouse Model; Airway Inflammationmentioning

confidence: 99%

Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

Hortobagyi

Kierstein

Krytska

et al. 2008

Journal of Allergy and Clinical Immunology

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“…Following immune excitation, memory/effector CD4 + Th2 cells then leave the draining lymph nodes and extravasate at sites of inflammation during the challenge phase. Once in the tissues, Th2 cells interact with IgE-bearing local DC to increase IL-4, IL-5, IL-9, and IL-13 production [90][91][92][96][97][98][99][100][101][102]. These cytokines are important for inducing tissue eosinophilia, airway hyperreactivity, and the production of chemokines that attract further inflammatory cells.…”

Section: The Impact Of Particulate Pollutants On Asthmamentioning

confidence: 99%

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Xia

Nel

2008

Free Radical Biology and Medicine

813

529

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Ambient particulate matter (PM) is an environmental factor that has been associated with increased respiratory morbidity and mortality. The major effect of ambient PM on the pulmonary system is the exacerbation of inflammation, especially in susceptible people. One of the mechanisms by which ambient PM exerts its proinflammatory effects is the generation of oxidative stress by its chemical compounds and metals. Cellular responses to PM-induced oxidative stress include activation of antioxidant defense, inflammation, and toxicity. The pro-inflammatory effect of PM in the lung is characterized by increased cytokine/chemokine production and adhesion molecule expression. Moreover, there is evidence that ambient PM can act as an adjuvant for allergic sensitization, which raises the possibility that long-term PM exposure may lead to increased prevalence of asthma. In addition to ambient PM, rapid expansion of nanotechnology has introduced the potential that engineered NP may also become airborne and may contribute to pulmonary diseases by novel mechanisms that could include oxidant injury. Currently, little is known about the potential adverse health effect of these particles. In this communication, the mechanisms by which particulate pollutants, including ambient PM and engineered NP, exert their adverse effects through the generation of oxidative stress and the impacts of oxidant injury in the respiratory tract will be reviewed. The importance of cellular antioxidant and detoxification pathways in protecting against particle-induced lung damage will also be discussed.

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“…Several investigators have shown that lung DC [9,43,54] or GM-CSF-cultured bonemarrow derived DC injected into the lung [55] are able to induce the typical Th2 response to inhaled allergen. Adoptive transfer studies showed that it is mainly the SIRPa 1 CD11b 1 lung DC that are efficient at Th2 priming, whereas Flt3L-cultured cDC are not [6,8].…”

Section: The Role Of Lung DC Subsets In Allergy and Asthmamentioning

confidence: 99%

Origin and functional specializations of DC subsets in the lung

2010

Self Cite

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Lung DC bridge innate and adaptive immunity, and depending on the context, induce Th1, Th2 or Th17 response, to optimally clear infections. Conversely, lung DC can also prevent overt and harmful immune responses to harmless inhaled antigens via induction of Treg cells or via induction of neutralizing mucosal IgA antibodies. Here, we propose that these functions are not the result of a single population of DC, and instead, subsets of DC perform specialized functions.

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Myeloid dendritic cells induce Th2 responses to inhaled antigen, leading to eosinophilic airway inflammation

Cited by 467 publications

References 42 publications

Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

Surfactant protein D inhibits TNF-α production by macrophages and dendritic cells in mice

The role of oxidative stress in ambient particulate matter-induced lung diseases and its implications in the toxicity of engineered nanoparticles

Origin and functional specializations of DC subsets in the lung

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