Asthma is a chronic inflammatory disease of the airways which makes the respiratory tract hyper-responsive. Exact mechanisms of asthma are complicated to pinpoint due to its heterogeneity of eosinophilic and non-eosinophilic asthma. However, abnormal accumulation of mast cells, eosinophils, dendritic cells, and basophils are thought to be the major cause of asthma, resultant in IgE mediated sensitization with Th-2 CD4+ lymphocytes secreting cytokines IL-2, IL-4, IL-5, IL-13, IL-17, and IFN-γ which causes more irritation and hyper-responsiveness. These cytokines, as well as IL-3, IL-9, IL-13, and IL-15 extend eosinophil survival as they reduce apoptosis. An imbalance between Th17 and Treg cells also plays a role in asthma. The objective for
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Chronic asthma leads to damage of the airway epithelium in which these drugs are unable to reverse. Presently, there is no treatment that targets the cytokines which cause non-eosinophilic asthma. Asthma is a disease that is estimated to affect 10-15% of the United States population. About two-thirds of all asthma cases are diagnosed in those under the age of 18, but it may also appear during adulthood. Asthma involves the airways in the lungs to become swollen and to spasm causing the individual to wheeze or gasp for air. Continuous inflammation causes the airways to become …show more content…
Regulatory T cells (Treg) maintain self-tolerance and act as an anti-inflammatory. Th17 cells are significant in the development of allergic reactions, NEA, and autoimmunity. Therefore, the elevated expression of IL-17 which is linked to hyper-responsiveness and the disequilibrium between Th17 and Treg cells may be a source for asthma (Furukawa et al. 2015). Antigen presenting cells (APC’s) also play a part in asthma since T lymphocytes cannot respond to antigens without the help of APC’s such as dendritic cells. Dendritic cells are able to initiate an immune response by stimulating naïve T cells. A combination of increased quantities of CD1a and increased expression of major histocompatibility complex class II (MHCII) (HLA-DR) has been found in patients with asthma (Möller et al. 1996). Another component to asthma is the abnormal accumulation of basophils, eosinophils, lymphocytes, mast cells, and antigen presenting cells. This results in T-helper 2 cells (Th2) secreting cytokines (Riccioni et al. 2004). These cytokines called interleukins such as IL-4, IL-5, and IL-13 which are derived from Th2 CD4+ cells and innate lymphoid cells are underlying factors of inflammatory processes (Chung et al. 2015). Those cytokines not only cause inflammation, but they also trigger various effects such as eosinophil recruitment, B cell IgE synthesis, and fibroblast activation (Kaur et al.
Chronic asthma leads to damage of the airway epithelium in which these drugs are unable to reverse. Presently, there is no treatment that targets the cytokines which cause non-eosinophilic asthma. Asthma is a disease that is estimated to affect 10-15% of the United States population. About two-thirds of all asthma cases are diagnosed in those under the age of 18, but it may also appear during adulthood. Asthma involves the airways in the lungs to become swollen and to spasm causing the individual to wheeze or gasp for air. Continuous inflammation causes the airways to become …show more content…
Regulatory T cells (Treg) maintain self-tolerance and act as an anti-inflammatory. Th17 cells are significant in the development of allergic reactions, NEA, and autoimmunity. Therefore, the elevated expression of IL-17 which is linked to hyper-responsiveness and the disequilibrium between Th17 and Treg cells may be a source for asthma (Furukawa et al. 2015). Antigen presenting cells (APC’s) also play a part in asthma since T lymphocytes cannot respond to antigens without the help of APC’s such as dendritic cells. Dendritic cells are able to initiate an immune response by stimulating naïve T cells. A combination of increased quantities of CD1a and increased expression of major histocompatibility complex class II (MHCII) (HLA-DR) has been found in patients with asthma (Möller et al. 1996). Another component to asthma is the abnormal accumulation of basophils, eosinophils, lymphocytes, mast cells, and antigen presenting cells. This results in T-helper 2 cells (Th2) secreting cytokines (Riccioni et al. 2004). These cytokines called interleukins such as IL-4, IL-5, and IL-13 which are derived from Th2 CD4+ cells and innate lymphoid cells are underlying factors of inflammatory processes (Chung et al. 2015). Those cytokines not only cause inflammation, but they also trigger various effects such as eosinophil recruitment, B cell IgE synthesis, and fibroblast activation (Kaur et al.