ANTI-Ige: An Overview

Asthma is common chronic inflammatory disease of the airways characterised by variable and attacks of cough and breathlesness, usually precipitated by an enviromental trigger (air pollution, smoke, etc). The prevalence and severity for allergic asthma have increased markedly in the last several decades. Dysregulated expression patterns of proand anti inflammatory mechanisms are thought to be responsible for the development of chronic inflammation. The risk of developing asthma has a strong genetic component, with estimated heritability ranging from 35 to 85%. The mechanism of action of Omalizumab in the treatment of asthma is believed to be multifactorial. and its dysregulated expression have been linked to atopic diseases such as atopic dermatitis, asthma, allergic rhinitis and eosinophilic esophagitis [6]. The response to drug treatment in asthma is a complex trait and is markedly variable even in patients with apparently similar clinical features. Pharmacogenomics, which is the study of variations of human genome characteristics as related to drug response, can play a role in asthma therapy. Both a traditional candidate-gene approach to conducting genetic association studies and genome-wide association studies have provided an increasing list of genes and variants associated with the three major classes of asthma medications: β2-agonists, inhaled corticosteroids, and leukotriene modifiers. Moreover, a recent integrative, systems-level approach has offered a promising opportunity to identify important pharmacogenomics loci in asthma treatment [7]. The polymorphisms within the ADRB2 gene that are potentially associated with obesity and asthma include Arg16Gly and Glu27Gln, and probably to some extent Thr164Ile, as well. The pleiotropic nature of ADRB2 makes it a good candidate for such an association. It also has an established role in the development of both conditions separately. The underlying mechanism seems to depend on both the alternations in lung function and the metabolic effect associated with ADRB2. However, it could also be linked to immunological functions related to ADRB2 expressions on leukocytes [8]. A genome-wide association study (GWAS) identified a previously unknown asthma-susceptibility locus on chromosome 17q21, harboring the adjacent genes ORMDL3 (ORMDL sphingolipid biosynthesis regulator 3) and GSDMB (Gasdermin B). This genetic association has been confirmed in ethnically diverse populations, and gene–environment interactions have been detected between susceptibility alleles and exposure to cigarette smoke and furred pets. Acevedo et al. showed that, significant differences in the DNA methylation levels of the ORMDL3promoter of asthmatic children, independent of age, gender, genotype and differential leukocyte cell counts, which might partially explain the increased ORMDL3 expression observed in cases. Their results Asthma and Genetic Factors Asthma is common chronic inflammatory disease of the airways characterised by variable and attacks of cough and breathlesness, usually precipitated by an enviromental trigger (air pollution, cold, dry air, smoke, etc). The prevalence and severity for allergic asthma have increased markedly in the last several decades. Dysregulated expression patterns of proand anti inflammatory mechanisms are thought to be responsible for the development of chronic inflammation. The sequence of immunopathogenesis is unclear but there is clearly a genetic predisposition. Asthma is caused by multiple interacting genes, some having a protective effect and others contributing to the disease pathogenesis, with each gene having its own tendency to be influenced by the environment. By the end of 2010, 100 genes had been associated with asthma in six or more separate populations, including GSTM1, IL-1 (α,β), IL-1RN, TSLP-R, IL-1R1, IL-8RA, IL3,4,5,9,10,12,13, NAT2, CTLA-4, SPINK5, V-CAM 1, TNF-α, ARG1, GSTM1, A3AR, CHIA, LELP1, TGFβ1, SOD-1, EGFR, GPRA, CCR2, FcεRIβ, PHF11, ACE, IRAK-3, CD69, IL-18, MUC-2, eNOS; NOS3, CMA1, and ADAM33, among others [1-3]. The risk of developing asthma has a strong genetic component, with estimated heritability ranging from 35 to 85% . Asthma is described as a complex disease arising from the contribution of multiple genetic and environmental factors [4,5]. Some of these genes may also be involved with other phenotypes such as helminthic infections (FcεRIβ and IL-4), COPD, cardiovascular diseases, congenital thrombotic thrombocytopenia, Crohn’s disease (ADAM33) renal cell carcinoma, blood malignancies (PHF11), tuberculosis (TB), hyperparathyroidism, prostate cancer, insulin dependent diabetes mellitus, leprosy and chronic hepatitis B infection (vitamin D receptor:VDR) [2]. Thymic stromal lymphopoietin (TSLP) is an epithelial-derived cytokine similar to IL7, whose gene is located on chromosome 5q22. 1 and it exerts its biological function through the TSLP-Receptor (TSLP-R). TSLP is expressed primarily by epithelial cells at barrier surfaces such as the skin, gut and lung in response to danger signals. TSLP genetic variants Review Article ANTI-Ige: An Overview Arzu Didem Yalcin* and Academia Sinica Genomics Research Center, Dr. Academia Sinica, 11529, Taipei, Taiwan, And Internal Medicine, Allergy and Clinical Immunology, Near East University, Nicosia, Cyprus Dates: Received: 29 October, 2014; Accepted: 03 December, 2014; Published: 05 December, 2014 *Corresponding author: Arzu Didem Yalcin MD. Genomics Research Center, Dr.Academia Sinica, 11529, Taipei, Taiwan, And Internal Medicine, Allergy and Clinical Immunology, Near East University, Nicosia, Cyprus, Tel: 8860278977509; E-mail: