GENETIC RISK FACTORS OF DEVELOPMENT ALLERGIC KID'S DISEASES

Kalyuzhka E. A.

LITERATURE REVIEWS

Scentific article

An analysis of numerous studies indicates multifactorial pathogenesis of allergic diseases, in which the demonstration involved both internal and external causes. Clinical and clinical-genetic studies allow us to confidently consider genetic factors predisposing major risk factor for atopic diseases. The presence of atopic disease in the family is considered with a genetic factor predisposing to the development of kid’s IgE-mediated hypersensitivity, and is a prerequisite for the determination of the newborn in the group of "high risk". Considering the genetic causes, we cannot exclude abnormal gene mutations that contribute to the dynamics of the incidence rate. At the same time, from 10 to 20% of children with allergic disorders have family history. Nowadays, not identified any genetic marker that would accurately predict the likelihood of developing allergic disease, so burdened hereditary history remains the only significant factor that allows you to select children with high risk to develop allergies. Genetically determined in atopic disease is the overproduction of IgE. Control IgE synthesis is carried Ir-genes and HLA system. The development of allergic reactions associated with three types of genetic regulation: regulation of IgE-synthesis is not associated with the major histocompatibility complex; genetic regulation associated with the major histocompatibility complex; specifying the functioning suppressor genes and genetic regulation associated with the severity of the immune response to antigenic exposure. 5a23-31 chromosome contains genes that control the levels of IgE, the level of IL4, IL13, inducing the synthesis of IgE, the synthesis of IL3, IL5, IL9, IL12, involved in the development of allergic inflammation, as well as the genes coding for the synthesis of glucocorticoid and β2 adrenergic receptor. An important function is to activate IL4 high affinity receptor for IgE FcεRl expression on B-lymphocytes. Besides, IL4 stimulates the production of B-lymphocyte adhesion molecules enhances cytolytic activity of CD8 lymphocytes, promotes the expression of MHC class II molecules on macrophages and monocytes, antigen-presenting macrophage activity enhances, inhibits the development of the colonies and macrophage release of IL1, IL12, IFNy. IL4 gene was localized to the short arm of chromosome in section 31.1 5. Several point detected polymorphisms in the promoter region of the gene IL4. Family inheritance of asthma and allergic disease suggests that genetic factors are important in the pathogenesis of allergy. However, reliable genetic markers specific IgE sensitization and allergic diseases has not yet been identified. Although a number of genes — "candidates" is already defined, role in the pathogenesis of the disease or of one of them has not yet been confirmed. Research on the interaction between different genes and between genes and the environment ("gene - gene", "gene - environment» - interaction) suggest that prevention of allergic diseases should be directed to the individual genetic vulnerabilities ("gene profile") and environmental impact factors. The analysis showed that nowadays has not identified any genetic marker that would accurately predict the likelihood of developing allergic disease. Undoubtedly is still the logical proof of the inheritance of a certain type immunological response, which can appear in several phenotypically atopic diseases in different age periods.

genetic factors, allergies, children

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