Allergic airway inflammation.
Several genes, including ADAM33, DPP10, PHF11, GPRA, and TIM-1, have been implicated in the pathogenesis and susceptibility to atopy and asthma. Advances have been made in defining the mechanism for the control of allergic airway inflammation in response to inhaled antigens. There is growing evidence that associates asthma with a systemic propensity for allergic type 2 T-cell cytokines. Disordered coagulation and fibrinolysis could also exacerbate asthma symptoms. Major emphasis on immunotherapy for asthma during the past decade has been to direct the immune response to a type 1 response. Recent literature supports the pivotal role of plasmacytoid dendritic cells and allergen-specific T-regulatory cells in the development of tolerance to allergens. In this review article, we discuss the current information on the pathogenesis of allergic airway inflammation and potential allergen immunotherapies, which could be beneficial in the treatment of airway inflammation, allergy, and asthma.
Agrawal
Devendra K
DK
Departments of Biomedical Sciences, Medicine, and Medical Microbiology and Immunology, Creighton University School of Medicine, CRISS I Room 131, 2500 California Plaza, Omaha, NE 68178, USA. dkagr@creighton.edu
Bharadwaj
Arpita
A
D001249:Asthma / Q000209:etiology* / Q000235:genetics / Q000276:immunology; D001777:Blood Coagulation; D018414:CD8-Positive T-Lymphocytes / Q000502:physiology; D003713:Dendritic Cells / Q000502:physiology; D006801:Humans; D015375:Receptors, Interleukin-2 / Q000032:analysis; D050378:T-Lymphocytes, Regulatory / Q000502:physiology; D018417:Th1 Cells / Q000276:immunology; D018418:Th2 Cells / Q000276:immunology
D015375:Receptors, Interleukin-2