| Autor: |
Brister DL; Division of Respirology, Department of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada., Omer H; Division of Respirology, Department of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada., Whetstone CE; Division of Respirology, Department of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada., Ranjbar M; Division of Respirology, Department of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada., Gauvreau GM; Division of Respirology, Department of Medicine, McMaster University, Hamilton, ON L8N 3Z5, Canada. |
| Abstrakt: |
Disruption of the airway epithelium triggers a defensive immune response that begins with the production and release of alarmin cytokines. These epithelial-derived alarmin cytokines, including thymic stromal lymphopoietin (TSLP), are produced in response to aeroallergens, viruses, and toxic inhalants. An alarmin response disproportionate to the inhaled trigger can exacerbate airway diseases such as asthma. Allergens inhaled into previously sensitized airways are known to drive a T2 inflammatory response through the polarization of T cells by dendritic cells mediated by TSLP. Harmful compounds found within air pollution, microbes, and viruses are also triggers causing airway epithelial cell release of TSLP in asthmatic airways. The release of TSLP leads to the development of inflammation which, when unchecked, can result in asthma exacerbations. Genetic and inheritable factors can contribute to the variable expression of TSLP and the risk and severity of asthma. This paper will review the various triggers and consequences of TSLP release in asthmatic airways. |
