Genetics of allergic disease

Holloway, John W.; Yang, Ian A.; Holgate, Stephen T.

doi:10.1016/j.jaci.2009.10.071

Cited by 204 publications

(107 citation statements)

References 133 publications

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“…Pathological analyses of the airway wall reveal the airway epithelium of asthmatics to be highly disorganised, with evidence of sloughing and denudation of the basement membrane, mucus cell metaplasia, airway epithelial cell (AEC) hyperproliferation and an impaired ability to undergo re-epithelisation [5]. This phenotype may, in part, be mediated by a combination of genetic and environmental factors affecting epithelial barrier function [115], immunopathology caused by an aberrant host response or an inability to clear microbial infections. Although some investigators have shown that the airway epithelium itself is unable to produce a robust IFN-I response [116,117], this phenotype has not been reproduced by others [118,119].…”

Section: Pdc-derived Paracrine Support For Structural Cellsmentioning

confidence: 99%

The plasmacytoid dendritic cell: at the cross-roads in asthma

et al. 2013

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The onset, progression and exacerbations of asthma are frequently associated with viral infections of the lower respiratory tract. An emerging paradigm suggests that this relationship may be underpinned by a defect in the host's antiviral response, typified by the impaired production of type I and type III interferons (IFNs). The failure to control viral burden probably causes damage to the lung architecture and contributes to an aberrant immune response, which together compromise lung function.Although a relatively rare cell type, the plasmacytoid dendritic cell dedicates much of its transcriptome to the synthesis of IFNs and is pre-armed with virus-sensing pattern recognition receptors. Thus, plasmacytoid dendritic cells are specialised to ensure early viral detection and the rapid induction of the antiviral state to block viral replication and spread. In addition, plasmacytoid dendritic cells can limit immunopathology, and promote peripheral tolerance to prevent allergic sensitisation to harmless antigens, possibly through the induction of regulatory T-cells. Thus, this enigmatic cell may lie at an important intersection, orchestrating the immediate phase of antiviral immunity to effect viral clearance while regulating tolerance.Here, we review the evidence to support the hypothesis that a primary defect in plasmacytoid dendritic function may underlie the development of asthma. @ERSpublications A review of the evidence on the role of plasmacytoid dendritic function in the development of asthma

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Section: Pdc-derived Paracrine Support For Structural Cellsmentioning

confidence: 99%

The plasmacytoid dendritic cell: at the cross-roads in asthma

et al. 2013

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“…Defects in skin barrier protein production evoke or aggravate atopic dermatitis by facilitating microbe penetration and contact of allergen and toxic chemicals (10). A loss of function mutation of filaggrin is associated with other allergic diseases, as well as atopic dermatitis (24). TARC is produced by keratinocytes and functions as a Th2 chemokine, which induces skin inflammation in atopic dermatitis (9).…”

Section: Discussionmentioning

confidence: 99%

Arazyme inhibits cytokine expression and upregulates skin barrier protein expression

Kim

Shin³

et al. 2013

Molecular Medicine Reports

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Abstract. In the present study, the inhibitory effect of arazyme on allergic inflammation was investigated by evaluating the alteration of cytokine production and expression of skin barrier proteins in immune and HaCaT human keratinocyte cells. THP-1 human monocytic and EoL-1 human eosinophilic cells were treated with Dermatophagoides pteronissinus extract (DpE). Monocyte chemotactic protein-1 (MCP-1)/CCL2, interleukin (IL)-6 and IL-8 increased following DpE treatment and arazyme significantly blocked the increase of MCP-1, IL-6 and IL-8 expression in cell types. Secretion of MCP-1, IL-6 and IL-8 induced by lipopolysaccharide in THP-1 cells was also inhibited by arazyme treatment. Arazyme inhibited the secretion of IL-6 and IL-8 due to phorbol 12-myristate 13-acetate and calcium ionophores in human mast cells. Arazyme blocked the secretion of thymus and activation-regulated chemokine (TARC)/CCL17, MCP-1, IL-6 and IL-8 due to tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) in HaCaT cells. TNF-α and IFN-γ suppressed the expression of skin barrier proteins, including filaggrin, involucrin and loricrin. By contrast, arazyme increased the expression of filaggrin, involucrin and loricrin. These results may contribute to the development of a therapeutic drug for the treatment of allergic diseases, including atopic dermatitis.

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“…Это гены цитокинов, гены главного комплекса гистосовместимости, гены ме диаторов воспаления, гены β2 адренорецепторов, гены ферментов биотрансформации ксенобиотиков (ФБК), гены, распознающие консервативные струк туры микроорганизмов, гены, регулирующие барьер ную функцию эпителия, гены, детерминирующие тканевый ответ на хроническое воспаление и др. [2,3]. С помощью полногеномных подходов обнаруже ны новые гены предрасположенности к БА, раскры вающие неизвестные ранее стороны патогенеза этого комплексного заболевания [3,4].…”

Section: оригинальные исследованияunclassified

“…Генотип TNFA* 308A/A у больных тяжелой БА также встречался с более вы сокой частотой, чем в контрольной группе (8,33 % vs 1,39 %) (p = 0,00015; OШ = 6,45 (95% ный ДИ -2,16-19,29). Значительная ассоциация аллеля TNFA* 308A с БА и тяжестью ее течения отмечается во многих исследованиях у индивидов европейского и азиатс кого происхождения [2,3].…”

Section: результаты и обсуждениеunclassified

Evaluation of a role of cytokine gene polymorphisms in development of bronchial asthma in the Republic of Bashkortostan

Карунас¹,

Федорова²,

Рамазанова³

et al. 2012

Pulʹmonologiâ (Mosk.)

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SummaryAsthma is one of the most common, severe and debilitating multifactorial diseases resulting from complex interaction between genes and environ mental factors. The aim of the present work was to analyze the association between cytokine gene polymorphisms and development of asthma in population of the Republic of Bashkortostan. A total of 638 patients with asthma and 366 healthy individuals were recruited in our investigation. In summary, the study of cytokine gene polymorphisms and gene gene interaction suggested an important role of TNFA, IL4, CCL11 and IL13 gene polymorphisms in the development of asthma in Bashkortostan population.

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Genetics of allergic disease

Cited by 204 publications

References 133 publications

The plasmacytoid dendritic cell: at the cross-roads in asthma

The plasmacytoid dendritic cell: at the cross-roads in asthma

Arazyme inhibits cytokine expression and upregulates skin barrier protein expression

Evaluation of a role of cytokine gene polymorphisms in development of bronchial asthma in the Republic of Bashkortostan

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