The course of allergen-induced leukocyte infiltration in human and experimental asthma

Lommatzsch, Marek; Julius, Peter; Kuepper, Michael; Garn, Holger; Bratke, Kai; Irmscher, Sabrina; Luttmann, Werner; Renz, Harald; Braun, Armin; Virchow, J. Christian

doi:10.1016/j.jaci.2006.02.034

Cited by 81 publications

(74 citation statements)

References 37 publications

(55 reference statements)

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“…Our initial data showed that an early event occurring at the inception of the clinical symptoms following allergen challenge was the appearance of CD69 ϩ CD4 ϩ T cells within the tissue of the conducting airways and lung parenchyma. These data are in agreement with recent studies showing a peak of 24 h for T cell recruitment into human airways following allergen challenge although mouse studies have shown a later peak for T cell recruitment into BAL fluid using a similar model of EAAD, perhaps reflecting a difference in the kinetics of T cell recruitment into tissue compartments as opposed to the airway lumen (29,30). Nevertheless, these data are consistent with the conclusion that the early stages of allergic inflammation are an allergen-specific, CD4…”

Section: Discussionsupporting

confidence: 92%

Allergic Airways Disease Develops after an Increase in Allergen Capture and Processing in the Airway Mucosa

Garnier

Wikström

Zosky

et al. 2007

The Journal of Immunology

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Airway mucosal dendritic cells (AMDC) and other airway APCs continuously sample inhaled Ags and regulate the nature of any resulting T cell-mediated immune response. Although immunity develops to harmful pathogens, tolerance arises to nonpathogenic Ags in healthy individuals. This homeostasis is thought to be disrupted in allergic respiratory disorders such as allergic asthma, such that a potentially damaging Th2-biased, CD4+ T cell-mediated inflammatory response develops against intrinsically nonpathogenic allergens. Using a mouse model of experimental allergic airways disease (EAAD), we have investigated the functional changes occurring in AMDC and other airway APC populations during disease onset. Onset of EAAD was characterized by early and transient activation of airway CD4+ T cells coinciding with up-regulation of CD40 expression exclusively on CD11b− AMDC. Concurrent enhanced allergen uptake and processing occurred within all airway APC populations, including B cells, macrophages, and both CD11b+ and CD11b− AMDC subsets. Immune serum transfer into naive animals recapitulated the enhanced allergen uptake observed in airway APC populations and mediated activation of naive allergen-specific, airway CD4+ T cells following inhaled allergen challenge. These data suggest that the onset of EAAD is initiated by enhanced allergen capture and processing by a number of airway APC populations and that allergen-specific Igs play a role in the conversion of normally quiescent AMDC subsets into those capable of inducing airway CD4+ T cell activation.

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Section: Discussionsupporting

confidence: 92%

Allergic Airways Disease Develops after an Increase in Allergen Capture and Processing in the Airway Mucosa

Garnier

Wikström

Zosky

et al. 2007

The Journal of Immunology

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“…6 Similar to the present study, several earlier studies reported neutrophil influx in response to allergen challenge in human asthma subjects. [24][25][26] One interpretation of neutrophil recruitment after allergen exposure is that endotoxin contamination of allergenic extracts or stimulation of TLR4/MD2 signaling by allergen-LPS complex could explain neutrophil recruitment after pulmonary allergen challenge in those studies and in the present study. 27,28 However several lines of evidence strongly indicate that endotoxin contamination/signaling cannot explain the observations in the present study.…”

Section: Discussionsupporting

confidence: 48%

MD2 Facilitates Pollen and Cat Dander-Induced Innate and Allergic Airway Inflammation

Hosoki

Itazawa

Boldogh

et al. 2016

Journal of Allergy and Clinical Immunology

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Background-The NHANES study identified several pollens and cat dander among the most common allergens that induce allergic sensitization and allergic diseases. We recently reported that ragweed pollen extract (RWPE) requires TLR4 to stimulate CXCL-mediated innate neutrophilic inflammation that facilitates allergic sensitization and airway inflammation. Myeloid differentiation protein-2 (MD2) is a TLR4 coreceptor, but its role in pollen and cat dander-induced innate and allergic inflammation has not been critically evaluated.

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“…Increases in some or all BAL Th2 cytokines have been measured following segmental allergen challenge (23,(37)(38)(39)(40). Because IL-4, IL-5, and IL-13 can be produced by other leukocytes, including eosinophils, basophils, and mast cells (41,42), increases in BAL Th2 cytokines may result from both T cell and non-T cell-derived sources.…”

Section: Discussionmentioning

confidence: 99%

Multiple Chemokine Receptors, Including CCR6 and CXCR3, Regulate Antigen-Induced T Cell Homing to the Human Asthmatic Airway

Thomas

Banerji

Medoff

et al. 2007

The Journal of Immunology

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Human allergic asthma is a chronic inflammatory disease of the airways thought to be driven by allergen-specific Th2 cells, which are recruited into the lung in response to inhaled allergen. To identify chemoattractant receptors that control this homing pattern, we used endobronchial segmental allergen challenge in human atopic asthmatics to define the pattern of chemoattractant receptor expression on recruited T cells as well as the numbers of recruited CD1d-restricted NKT cells and levels of chemokines in the bronchoalveolar (BAL) fluid. CD1d-restricted NKT cells comprised only a small minority of BAL T cells before or after Ag challenge. BAL T cells were enriched in their expression of specific chemoattractant receptors compared with peripheral blood T cells prechallenge, including CCR5, CCR6, CXCR3, CXCR4, and BLT1. Surprisingly, following segmental allergen challenge, no chemoattractant receptor was specifically increased. However, CCR6 and CXCR3, which were expressed on virtually all CD4+ BAL T cells prechallenge, were markedly decreased on all recruited BAL T cells following Ag challenge, suggesting that these receptors were internalized following encounter with ligand in the airway. Our data therefore suggests a role for CCR6 and CXCR3, in conjunction with other chemoattractant receptors, in the recruitment of inflammatory T cells into the BAL during the allergic asthmatic response.

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The course of allergen-induced leukocyte infiltration in human and experimental asthma

Cited by 81 publications

References 37 publications

Allergic Airways Disease Develops after an Increase in Allergen Capture and Processing in the Airway Mucosa

Allergic Airways Disease Develops after an Increase in Allergen Capture and Processing in the Airway Mucosa

MD2 Facilitates Pollen and Cat Dander-Induced Innate and Allergic Airway Inflammation

Multiple Chemokine Receptors, Including CCR6 and CXCR3, Regulate Antigen-Induced T Cell Homing to the Human Asthmatic Airway

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