Molecular genetics of allergic diseases

被引:84
|
作者
Ono, SJ [1 ]
机构
[1] Harvard Univ, Schepens Eye Res Inst, Boston, MA 02115 USA
[2] Harvard Univ, Brigham & Womens Hosp, Boston, MA 02115 USA
[3] Harvard Univ, Comm Immunol, Boston, MA 02115 USA
关键词
atopy; genome analysis; linkage; inflammation;
D O I
10.1146/annurev.immunol.18.1.347
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Allergic diseases affect approximately one third or the general population. This class of disease, characterized by elevated serum IgE levels and hypersensitivity to normally innocuous antigen, can manifest in practically any mucosal tissue or as a systemic response. A few examples of serious allergic diseases include asthma, dermatitis, bee sting allergy, food allergy, conjunctivitis, and severe systemic anaphylaxis. Taken together, allergic diseases constitute one of the major problems of modern day medicine. A considerable portion of the healthcare budget is expended in the treatment of allergic disease, and morbidity rates of inner city asthmatics are rising steadily. Due to the enormity of the problem, there has been a worldwide effort to identify factors that contribute to the etiology of allergic diseases. Epidemiologic studies of multigeneration families and large numbers of twins clearly indicate a strong genetic component to atopic diseases. At least two independently segregating disease-susceptibility genes are thought to come together with environmental factors to result in allergic inflammation in a particular tissue. On the basis of the strong genetic studies, multiple groups have attempted to identify disease-susceptibility genes via either a candidate gene approach or by genome-wide scans. Both of these approaches have implicated multiple regions in the human and mouse genomes, which are currently being evaluated as harboring putative atopy genes.
引用
收藏
页码:347 / 366
页数:20
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