Allergies are by definition immunological hypersensitivity reactions to substances (allergens), usually proteins, tolerated in defined dose by normal individuals (21). Allergic reactions are manifested in allergic diseases such as asthma, eczema, and rhinoconjuncti-vitis, each defined by a group of symptoms and signs. The life-impairing effect of these diseases varies from subtle to dominant. In addition to impairing physical health there may be an impact on social and emotional health, especially in childhood (22). Allergic symptoms can significantly disturb productivity in school and work where they are among the major causes of absenteeism. The personal and social economic burden is considerable (22-24). During the second half of the twentieth century the prevalence of allergic diseases has increased in epidemic proportions. The highest prevalence is in children and teenagers. With, on average, every fourth child affected, allergic diseases represent the most common chronic childhood illnesses in many countries (25,26). The reasons for this increase are not known (25,27).
There are many exceptions, but in most cases in established allergic disease the inflammatory cascade leading to the symptoms follows allergen contact at mucosal membranes in airways or gastrointestinal tract and is initiated through specific recognition by Immunoglobulin E (IgE) antibodies (27). Overactive T helper 2 (Th2) cells may be considered as the immunopathological cornerstone of these reactions (28). When, for example, pollen-derived aeroallergen is inhaled by a non-allergic subject the immune system reacts mildly by producing allergen-specific IgG2 and IgG4 antibodies. This is probably due to specific recognition and action, e.g., production of interferon (IFN)-g by T helper 1 cells (Th1) cells (28,29). In contrast, in allergic individuals Th2 cells typically infiltrate to the affected tissue and produce cytokines such as interleukins (IL)-4, -5, -9, and, -13. These cytokines promote the production of IgE antibodies, development and accumulation of mast cells, eosinophils, and basophils (the primary effector cells in allergic inflammation) as well as overproduction of mucus and airway hyper-responsiveness in asthma. Recognition of allergens by specific IgE antibodies on the surface of mast cells and basophils triggers these cells to release pre- and newly formed proinflammatory and vasoactive molecules (e.g., histamine) that may cause tissue damage and other detrimental effects. Eosinophilic inflammation contributes to the airway hyper-responsiveness (28).
It is clear that there is a hereditary trait that predisposes to the formation of allergen-specific IgE antibodies and development of allergic disease (27). This genetic predisposition, known as atopy, affects arguably as many as 30-50% of the world population (2,25,27). Although the immunopathological mechanisms in established allergic diseases are well characterized, it is poorly understood how and why atopy leads or does not lead to allergic sensitization and why only some sensitized individuals develop symptomatic allergic disease (30). Intriguingly, the immune responses to common environmental allergens are initially dominated by Th2 cells in all newborn infants but these responses are not suppressed in atopic infants during the first year of life (31,32). This is thought to be due to defects associated with atopy, for example, impaired production of IFN-g, which compromise the normal maturation of Th2 antagonistic Th1 responses. The major driving force for the Th1 maturation is considered to be the nature of the microbial exposure encountered after birth. Recent studies indicate that another type of T helper cells, collectively referred to as regulatory T cells (Tregs), may also be involved or even be the chief executers in natural suppression of Th2 mediated responses to environmental allergens. At least two types of Tregs have been shown to have this ability in humans: (1) CD4+CD25+ Tregs, which probably mediate their action primarily via production of immunosuppressive cytokines transforming growth factor (TGF)-b (also in membrane-bound form) and IL-10 and (2) IL-10 producing Tregs (33-35). Notably, there is indication that the numbers of allergen-specific Tregs may be lower and their suppressive ability defective in those subjects who become sensitized (36,37). Also, the mechanism of successful allergen-injection immunotherapy has been linked with induction of IL-10 Tregs that suppress Th2 responses and induce switching from IgE to IgG4 antibody (33).
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The human body And Todays chemical infested world. Here is a news flash You are not allergic to pollen, pet dander, or whatever it is that makes your body revolt Rather, your body just can not handle that one thing, what ever it is, anymore, due to the massive barrage of toxic chemicals you and everyone else are ingesting every single day.