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Innate resistance to allergic diseases
Hypersensitivity of the immune system causes common allergic diseases such as asthma, dermatitis and so on. The immune system is consisting of two systems, the innate immunity, and the adaptive immunity. The former responses and reacts fairly quick to foreign compounds such as allergens and pathogens, while the latter involves in a more delayed and specific process to identify the foreign compounds and prevent the further reactions of the diplomatic compounds. The innate immune system is known to play a dominant role in the host defense system for allergies. Different cell types, cytokines, and receptors involved in the innate immune system help to protect the human body from allergic diseases. Deficiency in the immune system will result in an increase risk of allergic diseases. Innate immune system uses different types of cells such as neutrophils, macrophages, dendritic cells, natural killer cells in conjunction with natural barriers (skin) and cytokines.

General mechanisms involved in the innate immunity
The activation of the innate immunity is caused by interaction between the allergens from external environments with the pattern recognition receptors, leading to chronic inflammation. The innate immunity activation results in the attraction of white blood cells such as macrophages which can eliminate and digest allergens to the response site, which mediated by T helper cells. Innate immune systems insist in all species of animals. The innate immune system is known as a non-specific first-line defense against different types of pathogens.

Innate immunity in airway inflammation
Airway inflammation is a reversible airflow obstruction, and is hyperresponsiveness. The most common airway allergic diseases is asthma. An T helper 2 cell immune activate response mast cells and basophils in the asthmatic ariways, leading to the production of IgE. Pattern recognition receptors can mediate responses to inhaled particles. The different kinds of pattern recognition receptors such as Toll-like receptors, and their downstream pathways are claimed to play a vital role in response to allergic airway inflammation and other infectious lung diseases such as COPD.

Innate immunity in skin inflammation
Low molecular weight chemicals and metal ions can cause skin inflammation. The contact allergens induce skin inflammation by encountering with pattern recognition receptors as the Toll-like receptors TLR2 and TLR4 and the NOD-like receptor NLRP3. Atopic dermatitis is a chronic inflammatory skin disease, and is caused by bacteria and viral infections. Dysfunction of the skin barrier can result in a higher frequency of bacterial and viral skin infections from dysfunction of innate responses. Keratinocytes play a vital role in limiting allergic reactions, by protecting skin from invading bacteria and pathogens. Dendritic cells also play a crucial role in detecting and processing allergens by releasing TNF and IL-17.

Deficiency of innate immunity in allergic diseases
The development of the innate immunity undergo prolonged periods of maturation, and can be fragile to external environmental exposures. Thus, epigenetic changes in gene expression may be caused, leading to an increase in the risk of asthma. Primary immunodeficiencies are the heterogeneous group of genetically inherited diseases, which influence the ability of innate immunity against bacteria and viral infections, autoimmunity and cancer.

Two epidermal filaggrin gene are known to be associated with atopic dermatitis by dysfunction. In AD patients, a disseminated viral infection, eczema herpeticum is widely diagnosed. The viral infection is caused by bypassing the viral recongintion nectin-1, lack of cathelicidin production by keratinocytes, and depletion of Type I IFN-producing plasmacytoid dendritic cells from atopic dermatitis skin.