الفهرس 
introductionOnly 14 pages are availabe for public view
 |  | from | 149 |  |  |
| | | from | 149 | | |
Abstract
Allergic asthma is a chronic pulmonary disease associated with bronchoconstriction and inflammation with many mediators and proinflammatory cytokines released from T lymphocytes, eosinophils, and basophils and play an important role in parthogenesis of asthma. Pathophysiology of asthma has been undergone great advances in the past decade particularly with the recognition of cytokinesand the roles they may take in orchestrating the local inflammatory response. The disease is thought to originate as a result of polarized immune response to ubiquitous inhaled antigens. Ample evidence suggests that asthmatic lung is populated by CD4+ T cells predominantly of Th2 cytokine pattern results in recruitment of a number of effector cells (mast cells and eosinophils) which leads to the functional characteristics of the disease namely airway obstruction and hyperresponsiveness . structural changes also include epithelial desquamation, mucus cell hyperplasia, muscle hypertrophy and subepithelial fibrosis. The underlying cause of the abnormal immune response to common environmental antigens is not well-understood. Recently 2 cytokines Il-12, IL-13 have been proposed to play pivotal role in the aberrant immune response to inhaled allergens. Elevation of lung level of IL-13 and reciprocal impairment in IL-12 levels have been associated with the disease.