Allergy was originally defined in 1906 in 1906 by Clemens von Pirquet as 'altered reactivity' to denote the different reaction which on second exposure to and antigen due to the formation fo antibodies, when compared to the first exposure. The
term
atopy decribes the clinical presentation of Type I hypersensitivity, which include asthna, eczema, hay fever and urticaria, These usually occur in subjects with a family history of these or similar conditions. The mechanism of allergy is the Type
I
hypersensitity reaction. contact with allergen results in its being processed by an antigen presenting cell and presented to T helper cells which then help B cells to IgE antibody. The IgE antibody is rapidly taken up via its Fc portion by mast
cells
and basophils, which are then senitized. Subsequent contact with same allergen will result in the cross-linking of IgE molecules by their fab portions which cause cell degranulation and mediator release.
The contribution of genentic factors to the development of atopy has been an intriguing issue. The exact controlling mechanisms of the genetic factors are unknown, but there are many studies support the genetic controls of the development of
atopy.
Abnormally high levels of IgE synthesis and associated atopy often run in families. Althouth the full inhritance pattern is probably multigenic, family studies has shown that their is clear autosomal transmission of atopy. The ability to make
specific
IgE antibodies to certain antigens, e.g., ragweed pollen, is also inherited and may be linked to particular class II major histocompatibility complex alleles.
Therefore, I think that the clinicians must consider the environmental and genetic factors when evaluate the atopic disease.
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