Epigenetics of allergic diseases

Allergic diseases including asthma, allergic rhinitis, food allergies, and eczema (atopic dermatitis) have increased worldwide in the past four decades. The increase seems to result from gene–environment interactions, leading to epigenetic changes during critical development periods. Four epigenetic mechanisms have been identified: DNA methylation (DNAm), histone modification, chromatin remodeling, and noncoding RNAs. Most prior studies have focused on DNAm. Immune responses are mediated by T and B lymphocyte cells. B cells and their antibodies (immunoglobulins) constitute humoral immunity; T cells provide cell-mediated immunity. An atopy/allergy is a misguided immune response to low doses of allergens and can develop to asthma, allergic rhinitis, or eczema. Hallmarks of eczema are skin barrier defects and immunologic dysregulation characterized by intense itching, chronically relapsing, and recurrent lesions of inflammatory skin. For asthma, shortness of breath and wheezing or whistling in the chest are first symptoms. Food protein allergens can cause clinical symptoms that range in their severity from mild itching to severe and fatal anaphylaxis. Allergic rhinitis is driven by airborne allergens and is characterized by sneezing, a runny or a blocked nose without a cold. The evidence of epigenetic risk factors for allergic disorders varies. Specific markers of allergic response, such as skin prick test and specific immunoglobulins, vary widely with age. Thus, only few epigenetic risks could be identified. Research on eczema is severely hampered by an unnecessary scientific dispute between approaches that either focused on the skin (barrier function) or on immune responses. The epigenetics of asthma is well developed. More than 30 epigenetic markers have been identified in two independent studies, and future applications in clinical science can be expected. An insufficient number of studies have researched epigenetics of allergic rhinitis.