儿童哮喘危险因素和TIM基因多态性分析-儿科学专业论文.docxVIP

Study on the PolymorPhisms of childhood asthma gene TIM family and Relative Factors Abstract Background:Asthma is the most common chronic respiratory allergic disease in childhood, and in recent years its prevalence has increased worldwide [1, 2]. Asthma is a complex disease of multifactorial etiologies including environmental factors and an obvious genetic element [3]. Prevalence of asthma reported in various countries and regions have great McIntire et al. [4] discovered a Tapr (T cell and airway phenotype regulator) on mous chromosome 11, which can regulate the T cell and airway phenotype, and found a novel gene TIM (T cell immunoglobulin domain and mucin domain) family. TIM-1, TIM-2, and TIM-3 were found to be members of the TIM gene family located on chromosome 5q33.2 [5-7] . This is also one of the major genetic susceptibility sites for asthma. TIM protein is a type I transmembrane protein encoded by the TIM gene, including an N-terminal Ig V region (IgV) domain, a mucin-like domain, a transmembrane domain, and a cytoplasmic tail with a phosphorylation motif [8]. The TIM gene family plays a critical role in development of allergic disorders such as asthma and autoimmune diseases [9]. TIM-1, first molecule in the TIM family and the most important one, was first found in renal cells of the African Green Monkey [10]. In subsequent studies, it was confirmed to be the same molecule as the human hepatitis A virus receptor, hHAVcr-1[11], and the kidney injury molecule 1 (KIM-1) [12]. TIM-1 is selectively expressed on activated CD4+T cell surfaces, especially on Th2 cells, and regulates the Th2-type cell-mediated immune response (4, 6). It also has an effect on macrophages involved in local inflammation [13]. TIM-3 molecules are expressed mainly on the surfaces of Th1 cells causing a negative effect on the regulation of those cells [14, 15] As the natural ligand of TIM-1, TIM-4 is exclusively expressed on the surf