Amin Zakeri1, Fariba Ghiamati Yazdi2. 1. Immunology Section, Department of Pathobiology, Faculty of Veterinary Medicine, Ferdowsi University of Mashhad, Mashhad, Iran. Electronic address: Amin.zakeri@stu-mail.um.ac.ir. 2. Department of Food Science and Technology, Faculty of Agriculture, Isfahan University of Technology, Isfahan 84156, Iran.
Abstract
BACKGROUND: Innate immune cells as the first line of defense are adept at recognizing and triggering appropriate response against various pathogens. Apart from the protective functions, the innate immunity plays an essential role in mediation of allergic responses. Dendritic cells (DCs) and airway epithelial cells (AECs) along with other innate cells such as granulocytes, natural killer cells (NKs), natural killer T cells (NKTs), and alternatively activated macrophages (AAMs) are able to orchestrate allergic responses, especially asthma. Chronic stimulation of TLRs by airway stimuli induces local inflammation which gradually results in the recruitment and settling of innate cells around airways. SCOPE OF REVIEW: This review discusses how recruitment and accumulation of the inflammatory cells in the site of insult facilitate hypersensitivity reactions and initiate airway inflammation. We indicate that these cells are well equipped to highly sensitive receptors known as toll-like receptors (TLRs) making them fit to prime adaptive immune response. Based on emerging findings, we highlight the pivotal role of TLRs in regulation of innate cells function in the context of asthma disease. MAJOR CONCLUSIONS: Stimulation of the TLRs of innate cells by allergens has been found to accelerate and regulate allergic airway inflammation. In fact, the sophisticated interaction between environmental allergens and TLRs leads to release of various pro-inflammatory mediators from innate cells supporting asthma development. GENERAL SIGNIFICANCE: This review highlights that TLRs have a substantial role in priming innate cells and cytokine release, suggesting that the involvement of TLRs of innate immune cells can modulate the function of these cells in asthma disease. Copyright Â
BACKGROUND: Innate immune cells as the first line of defense are adept at recognizing and triggering appropriate response against various pathogens. Apart from the protective functions, the innate immunity plays an essential role in mediation of allergic responses. Dendritic cells (DCs) and airway epithelial cells (AECs) along with other innate cells such as granulocytes, natural killer cells (NKs), natural killer T cells (NKTs), and alternatively activated macrophages (AAMs) are able to orchestrate allergic responses, especially asthma. Chronic stimulation of TLRs by airway stimuli induces local inflammation which gradually results in the recruitment and settling of innate cells around airways. SCOPE OF REVIEW: This review discusses how recruitment and accumulation of the inflammatory cells in the site of insult facilitate hypersensitivity reactions and initiate airway inflammation. We indicate that these cells are well equipped to highly sensitive receptors known as toll-like receptors (TLRs) making them fit to prime adaptive immune response. Based on emerging findings, we highlight the pivotal role of TLRs in regulation of innate cells function in the context of asthma disease. MAJOR CONCLUSIONS: Stimulation of the TLRs of innate cells by allergens has been found to accelerate and regulate allergic airway inflammation. In fact, the sophisticated interaction between environmental allergens and TLRs leads to release of various pro-inflammatory mediators from innate cells supporting asthma development. GENERAL SIGNIFICANCE: This review highlights that TLRs have a substantial role in priming innate cells and cytokine release, suggesting that the involvement of TLRs of innate immune cells can modulate the function of these cells in asthma disease. Copyright Â
Authors: Vanitha Sampath; Dana Tupa; Michelle Toft Graham; Talal A Chatila; Jonathan M Spergel; Kari C Nadeau Journal: Ann Allergy Asthma Immunol Date: 2017-01 Impact factor: 6.347