الفهرس 
Age distribution of the study groupsOnly 14 pages are availabe for public view
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Abstract
The development of allergic rhinitis (AR) is caused by the interaction between genetic predisposition and environmental factors.
The etiology and pathogenesis of nasal polyps is a matter of vigorous debate, bacteria, viruses, and fungi have all been suggested as potential contributors to the development of the inflammatory process. Research on NPs have also persuasively demonstrated that an abnormal immune-inflammatory response is the pathological process
Recent investigations have begun to identify genes that might be involved in AR The genes encoding cytokines and receptors in patients with AR were investigated the most .
several studies have investigated single-nucleotide polymorphisms (SNPs) in genes encoding the molecules implicated in the pathogenesis of allergic rhinitis and sinonasal polyps : including specific interleukins (ILs) and their receptors. Until recently it has been assumed that development and manifestation of allergic airway disease was primarily influenced by the activity of T helper (Th)1, Th2 cells and T-regulatory (Treg) cells in genetically susceptible individuals ..
Interleukin-21 (IL-21) cytokine is a member of the IL2 family mainly produced by CD4+ T cells and natural killer T cells (NKT) .
The IL2/IL21 region, located on chromosome 4q27, has shown increasing evidence of association with a number of autoimmune diseases including type 1 diabetes (T1D), ulcerative colitis (UC), Crohn’s disease, juvenile idiopathic arthritis (JIA) ,psoriatic arthritis and systemic lupus erythematosus (SLE) .