Abstract
Atopic asthma is a chronic inflammatory pulmonary disease characterised by recurrent episodes of wheezy, laboured breathing with an underlying Th2 cell-mediated inflammatory response in the airways. It is currently treated and, more or less, controlled depending on severity, with bronchodilators e.g. long-acting beta agonists and long-acting muscarinic antagonists or anti-inflammatory drugs such as corticosteroids (inhaled or oral), leukotriene modifiers, theophyline and anti-IgE therapy. Unfortunately, none of these treatments are curative and some asthmatic patients do not respond to intense anti-inflammatory therapies. Additionally, the use of long-term oral steroids has many undesired side effects. For this reason, novel and more effective drugs are needed. In this review, we focus on the CD4+ Th2 cells and their products as targets for the development of new drugs to add to the current armamentarium as adjuncts or as potential stand-alone treatments for allergic asthma. We argue that in early disease, the reduction or elimination of allergen-specific Th2 cells will reduce the consequences of repeated allergic inflammatory responses such as lung remodelling without causing generalised immunosuppression.
Highlights
Asthma is a serious chronic inflammatory lung disease characterised by recurrent episodes of wheezy laboured breathing with prolonged expiration accompanied by dry coughing and viscous mucus
Regulation of Fas ligand (FasL) plays an important role because FasLexpressing T cells are pivotal during the resolution of airway inflammation [98] and intratracheal delivery of Dendritic cells (DCs) co-transfected with FasL and allergen genes before
Th2 cells and/or their secreted effector molecules mediate the immune response to allergens and are triggered by exposure to specific allergens leading to allergic asthma
Summary
Asthma is a serious chronic inflammatory lung disease characterised by recurrent episodes of wheezy laboured breathing with prolonged expiration accompanied by dry coughing and viscous mucus. Numerous microRNAs play important roles in asthma [46] and selective inhibition of these molecules can be utilised to target development of Th2 cells. TSLP skews DCs to express high levels of OX40 ligand, which promotes the generation of Th2 cells [38]; its inhibition prevents Th2-mediated airway inflammation in mice [39]. CXCR4 is involved in Th2 cell migration into the lungs [58] and treatment of allergic mice with selective CXCR4 inhibitors significantly reduces AHR and inflammatory responses [59,60], supporting the further development of CXCR4 antagonists for asthma treatment. A pan-selectin inhibitor is currently in phase IIa clinical trials for COPD, might be promising for asthma [81] None of these adhesion molecules is selectively expressed on Th2 cells. Regulation of FasL plays an important role because FasLexpressing T cells are pivotal during the resolution of airway inflammation [98] and intratracheal delivery of DCs co-transfected with FasL and allergen genes before
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