Version 1
: Received: 25 May 2021 / Approved: 26 May 2021 / Online: 26 May 2021 (08:17:01 CEST)
How to cite:
Dargahi, M.; Taheri, N.; Mirsanei, Z.; Rasti, A.; Jafari, R. The Dual Role of Toll-like Receptor10. Preprints2021, 2021050625. https://doi.org/10.20944/preprints202105.0625.v1
Dargahi, M.; Taheri, N.; Mirsanei, Z.; Rasti, A.; Jafari, R. The Dual Role of Toll-like Receptor10. Preprints 2021, 2021050625. https://doi.org/10.20944/preprints202105.0625.v1
Dargahi, M.; Taheri, N.; Mirsanei, Z.; Rasti, A.; Jafari, R. The Dual Role of Toll-like Receptor10. Preprints2021, 2021050625. https://doi.org/10.20944/preprints202105.0625.v1
APA Style
Dargahi, M., Taheri, N., Mirsanei, Z., Rasti, A., & Jafari, R. (2021). The Dual Role of Toll-like Receptor10. Preprints. https://doi.org/10.20944/preprints202105.0625.v1
Chicago/Turabian Style
Dargahi, M., Arezoo Rasti and Reza Jafari. 2021 "The Dual Role of Toll-like Receptor10" Preprints. https://doi.org/10.20944/preprints202105.0625.v1
Abstract
Toll-like receptors (TLRs) are a class of pattern recognition receptors (PRRs) family that identify pathogen-associated molecular patterns derived from microbes and activate immune cell response. Following TLRs ligation, different adaptor and transcription molecules such as myeloid differentiation primary response gene 88 (MyD88) and nuclear factor kappa B (NF-kB) are recruited that initiate inflammatory signaling pathways. The human Toll-like receptor 10 (hTLR10) is a novel member of the PRRs family with a regulatory function of immune responses because of unique cytoplasmic domains which lead to induction of both inflammatory and anti-inflammatory properties. Recent studies have reported the association of TLR10 polymorphisms with many inflammatory diseases and human cancer. Engagement of TLR10 on the surface of the epithelium and macrophages leads to the production of proinflammatory cytokines and chemokines, while other studies have proven an anti-inflammatory role of TLR10. Accordingly, TLR10 suppresses proinflammatory cytokine production via negative regulation of MyD88 and the Akt (protein kinase B) and MAPK (mitogen-activated protein kinase) signaling pathways. This review aimed to provide answers for these conflicting findings (Inflammatory and anti-inflammatory properties of TLR10) to further identify distinct biological functions of TLR10.
Copyright:
This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
