Allergic inflammation underlies several diseases such as asthma, rhinitis, and atopic dermatitis).It involves a great array of cells and molecules of innate and adaptive immunity.Components of the innate inflammatory pathways, among them epithelium receptors, alarmins and ILC2, are the earliest participants in some inflammatory processes, mainly the house dust mite induced bronchial inflammation in asthma.The importance of innate mechanisms, not only as a necessary step for inducing adaptive Th2 response but also to maintain chronic inflammation, is being increasingly recognized in recent years.In addition, the specificity of the Th2 cells and IgE is not only a crucial component of allergic inflammation but allows also identification of the causal inducers and their effects on eosinophils, neutrophils, and basophils recruitment and activation.The regulatory mechanisms of the allergic responses include Treg and Breg activity but the most important action to control this process is stopping the specific allergen exposure.However, this is very difficult to achieve in asthma because, in general, not all the allergens involved can be identified; in addition, nonimmune pathways play also a role.Since most people exposed to proallergic environments do not develop allergic diseases and it is well known that these conditions run in families, their genetic and epigenetic influences are a matter of intensive research.In this review we make an update of the basic mechanisms of allergic inflammation, trying to identify important pathways that involve both innate and adaptive immunity, including environmental factors that can modify important regulators of immunity such as intestinal microbiota and air pollution.
Caraballo et al. (Thu,) studied this question.