Pathogenesis of allergic airway inflammation

Devendra K. Agrawal, Zhifei Shao

    Research output: Contribution to journalReview articlepeer-review

    106 Scopus citations

    Abstract

    Advances have been made in defining the mechanisms for the control of allergic airway inflammation in response to inhaled antigens. Several genes, including ADAM33, DPP10, PHF11, GPRA, TIM-1, PDE4D, OPN3, and ORMDL3, have been implicated in the pathogenesis and susceptibility to atopy and asthma. Growing evidence associates asthma with a systemic propensity for allergic T-helper type 2 cytokines. Disordered coagulation and fibrinolysis also exacerbate asthma symptoms. Balance among functionally distinct dendritic cell subsets contributes to the outcome of T-cell-mediated immunity. Allergen-specific T-regulatory cells play a pivotal role in the development of tolerance to allergens and immune suppression. The major emphasis on immunotherapy for asthma during the past decade has been to direct the immune response to a type 1 response, or immune tolerance. In this review, we discuss the current information on the pathogenesis of allergic airway inflammation and potential immunotherapy, which could be beneficial in the treatment of airway inflammation, allergy, and asthma.

    Original languageEnglish
    Pages (from-to)39-48
    Number of pages10
    JournalCurrent Allergy and Asthma Reports
    Volume10
    Issue number1
    DOIs
    StatePublished - Jan 2010

    All Science Journal Classification (ASJC) codes

    • Immunology and Allergy
    • Pulmonary and Respiratory Medicine

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