PMID- 27543676 OWN - NLM STAT- MEDLINE DCOM- 20171103 LR - 20180917 IS - 0304-4165 (Print) IS - 0304-4165 (Linking) VI - 1861 IP - 1 Pt A DP - 2017 Jan TI - Toll-like receptor-mediated involvement of innate immune cells in asthma disease. PG - 3270-3277 LID - S0304-4165(16)30290-2 [pii] LID - 10.1016/j.bbagen.2016.08.009 [doi] AB - 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. CI - Copyright A(c) 2016 Elsevier B.V. All rights reserved. FAU - Zakeri, Amin AU - Zakeri A AD - Immunology Section, Department of Pathobiology, Faculty of Veterinary Medicine, Ferdowsi University of Mashhad, Mashhad, Iran. Electronic address: Amin.zakeri@stu-mail.um.ac.ir. FAU - Yazdi, Fariba Ghiamati AU - Yazdi FG AD - Department of Food Science and Technology, Faculty of Agriculture, Isfahan University of Technology, Isfahan 84156, Iran. LA - eng PT - Journal Article PT - Review DEP - 20160817 PL - Netherlands TA - Biochim Biophys Acta Gen Subj JT - Biochimica et biophysica acta. General subjects JID - 101731726 RN - 0 (Toll-Like Receptors) SB - IM MH - Animals MH - Asthma/*immunology MH - Cell Communication MH - Humans MH - *Immunity, Innate MH - Models, Biological MH - Th2 Cells/immunology MH - Toll-Like Receptors/*metabolism OTO - NOTNLM OT - Allergen OT - Asthma OT - Innate immune cells OT - Toll-like receptors (TLRs) EDAT- 2016/08/21 06:00 MHDA- 2017/11/04 06:00 CRDT- 2016/08/21 06:00 PHST- 2016/06/08 00:00 [received] PHST- 2016/08/15 00:00 [accepted] PHST- 2016/08/21 06:00 [pubmed] PHST- 2017/11/04 06:00 [medline] PHST- 2016/08/21 06:00 [entrez] AID - S0304-4165(16)30290-2 [pii] AID - 10.1016/j.bbagen.2016.08.009 [doi] PST - ppublish SO - Biochim Biophys Acta Gen Subj. 2017 Jan;1861(1 Pt A):3270-3277. doi: 10.1016/j.bbagen.2016.08.009. Epub 2016 Aug 17.