A New Decade of ME Research: The 11th Invest in ME International ME Conference 2016
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2014, fungal exstracts detected in eosinophilic chronic rhinosinusitis induced cytokines from nasal

Discussion in 'Fungal Infection (Yeast, Candida)' started by osisposis, Jun 16, 2015.

  1. osisposis

    osisposis Senior Member

    2014, fungal exstracts detected in eosinophilic chronic rhinosinusitis induced cytokines from nasal polyp cells

    J Allergy Clin Immunol. 2008 Feb;121(2 Suppl):S393-7; quiz S418. doi: 10.1016/j.jaci.2007.07.039.
    7. Immunologic lung disease.
    Greenberger PA1.

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    The lung is an extremely complex organ and participates in initial responses to inhaled antigens, infectious agents, and irritants or as a response to exposure through the oral, parenteral, or transdermal routes. There can be constriction of the airways or involvement or even destruction of the lung parenchyma, depending on the condition. This review focuses on selected aspects of the pulmonary innate and adaptive immune responses; the new condition World Trade Center cough, which can cause an asthma-like presentation and resemble reactive airways dysfunction syndrome; and the diagnosis and treatment of various immunologic lung conditions. Innate immune responses occur in the acute respiratory distress syndrome and in transfusion-related acute lung injury. Adaptive immune responses involve specialized mucosal and systemic immune responses, lymphocytes, and antibodies and can result in CD4+ TH1 and TH2 phenotypes, such as TH1 for tuberculosis and TH2 for asthma.

    Immunol Rev. 2014 Jul;260(1):129-44. doi: 10.1111/imr.12183.
    Directing traffic: IL-17 and IL-22 coordinate pulmonary immune defense.
    McAleer JP1, Kolls JK.

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    Respiratory infections and diseases are among the leading causes of death worldwide, and effective treatments probably require manipulating the inflammatory response to pathogenic microbes or allergens. Here, we review mechanisms controlling the production and functions of interleukin-17 (IL-17) and IL-22, cytokines that direct several aspects of lung immunity. Innate lymphocytes (γδ T cells, natural killer cells, innate lymphoid cells) are the major source of IL-17 and IL-22 during acute infections, while CD4(+) T-helper 17 (Th17) cells contribute to vaccine-induced immunity. The characterization of dendritic cell (DC) subsets has revealed their central roles in T-cell activation. CD11b(+) DCs stimulated with bacteria or fungi secrete IL-1β and IL-23, potent inducers of IL-17 and IL-22. On the other hand, recognition of viruses by plasmacytoid DCs inhibits IL-1β and IL-23 release, increasing susceptibility to bacterial superinfections. IL-17 and IL-22 primarily act on the lung epithelium, inducing antimicrobial proteins and neutrophil chemoattractants. Recent studies found that stimulation of macrophages and DCs with IL-17 also contributes to antibacterial immunity, while IL-22 promotes epithelial proliferation and repair following injury. Chronic diseases such as asthma and chronic obstructive pulmonary disease have been associated with IL-17 and IL-22 responses directed against innocuous antigens. Future studies will evaluate the therapeutic efficacy of targeting the IL-17/IL-22 pathway in pulmonary inflammation.
    © 2014 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.

    J Allergy Clin Immunol. 2012 Jan;129(1):216-27.e1-6. doi: 10.1016/j.jaci.2011.10.036. Epub 2011 Nov 25.
    Innate lymphoid cells responding to IL-33 mediate airway hyperreactivity independently of adaptive immunity.
    Kim HY1, Chang YJ, Subramanian S, Lee HH, Albacker LA, Matangkasombut P, Savage PB, McKenzie AN, Smith DE, Rottman JB, DeKruyff RH, Umetsu DT.

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    Asthma has been considered an immunologic disease mediated by T(H)2 cells and adaptive immunity. However, clinical and experimental observations suggest that additional pathways might regulate asthma, particularly in its nonallergic forms, such as asthma associated with air pollution, stress, obesity, and infection.
    Our goal was to understand T(H)2 cell-independent conditions that might lead to airway hyperreactivity (AHR), a cardinal feature of asthma.
    We examined a murine model of experimental asthma in which AHR was induced with glycolipid antigens, which activate natural killer T (NKT) cells.
    In this model AHR developed rapidly when mice were treated with NKT cell-activating glycolipid antigens, even in the absence of conventional CD4(+) T cells. The activated NKT cells directly induced alveolar macrophages to produce IL-33, which in turn activated NKT cells, as well as natural helper cells, a newly described non-T, non-B, innate lymphoid cell type, to increase production of IL-13. Surprisingly, this glycolipid-induced AHR pathway required not only IL-13 but also IL-33 and its receptor, ST2, because it was blocked by an anti-ST2 mAb and was greatly reduced in ST2(-/-) mice. When adoptively transferred into IL-13(-/-) mice, both wild-type natural helper cells and NKT cells were sufficient for the development of glycolipid-induced AHR.
    Because plant pollens, house dust, and some bacteria contain glycolipids that can directly activate NKT cells, these studies suggest that AHR and asthma can fully develop or be greatly enhanced through innate immune mechanisms involving IL-33, natural helper cells, and NKT cells.
    Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.
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