Abstract

Allergic diseases are an adverse reaction of the immune system against otherwise innocuous substances and are characterized by their high complexity. Patients can be asymptomatic or their involvement could be as severe as asthma. The complex nature of the phenotypes involved seems to point to genetic and environmental factors implication. Familiar aggregation or genetic implication in the development of these diseases is well reported, and experts seem to agree that atopic diseases affect homozygotic twins more than dizigotic twins (Ownby, 1990, Duffy et al., 1990). Allergic diseases are characterized by a Th2 inflammatory response involving several possible modulator factors (genetics and environmental factors), subject-related or antigenrelated modulators such as adjuvants, solubility in the microenvironment of mucosa, size of the sensitization agent, mucosa permeability, viral infections, and the greater or lesser ability of effectors cells to liberate mediators. Other factors include atmospheric pollution, exposure to tobacco, lifestyle-related diet and hygiene habits and maternal effects. The interaction between these factors produces the clinical picture of allergic disease. Great advances have been performed in the understanding, diagnosis and treatment of these diseases but the search of specific protective or risk biomarkers is an unsolved field. Since completion of the human genome project a rapid progress in genetics and bioinformatics have enabled the development of multiple tools as well as a large public databases, which include genetic and genomic data linked to clinical health data. The scientific revolution represented by the description of the human genome was largely facilitated by the use of DNA microarray technology, which made it possible to build a catalog of all genes within a given organism. The human genome project found that humans have an average of between 20,000 and 25,000 protein-coding genes (IHGSC, 2004). In addition, genetic variability between individuals is approximately 1% (Venter et al., 2001), suggesting that interactions between genes, proteins and the environment contribute to differences in human phenotype, maintenance of health and susceptibility to disease. On the other hand, the emergence of gene expression microarray technology in the mid-1990s has enabled genome-wide measurement of gene expression in a single experiment. This is turn

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