Abstract
Simple SummaryDue to the broad functions of Toll-like receptor 2 (TLR2) in innate immunity, the drive for the development of TLR2-targeted therapeutic treatments has accelerated in recent decades. However, its dual role in both the activation and suppression of innate immune responses makes it very difficult to use the results from gathered basic research and apply them to the development of clinical trials. Therefore, this review aims to summarize the knowledge of the function of TLR2 in innate immunity and metabolism to provide some future research directions.Innate immunity is considered the first line of defense against microbial invasion, and its dysregulation can increase the susceptibility of hosts to infections by invading pathogens. Host cells rely on pattern recognition receptors (PRRs) to recognize invading pathogens and initiate protective innate immune responses. Toll-like receptor 2 (TLR2) is believed to be among the most important Toll-like receptors for defense against mycobacterial infection. TLR2 has been reported to have very broad functions in infectious diseases and also in other diseases, such as chronic and acute inflammatory diseases, cancers, and even metabolic disorders. However, TLR2 has an unclear dual role in both the activation and suppression of innate immune responses. Moreover, in some studies, the function of TLR2 was shown to be controversial, and therefore its role in several diseases is still inconclusive. Therefore, although TLR2 has been shown to have an important function in innate immunity, its usefulness as a therapeutic target in clinical application is still uncertain. In this literature review, we summarize the knowledge of the functions of TLR2 in host–mycobacterial interactions, discuss controversial results, and suggest possibilities for future research.
Highlights
Evidence suggests that recognition can be indirect, for instance, by the involvement of high-mobility group box 1 protein (HMGB1), which is a widely studied endogenous danger signal that induces inflammatory response through its interaction with danger-associated molecular patterns (DAMPs) recognized by Toll-like receptor 2 (TLR2), TLR4, and TLR9 [44,45]
We found that fewer leucocytes were recruited to wounded tail fin tissue in both tlr2 mutant and myd88 mutant zebrafish larvae, which suggests tlr2 and myd88 are involved in responses to tail wounding [71]
The recombinant PPE18 protein, which is a TLR2 ligand derived from Mycobacterium tuberculosis (Mtb), has been demonstrated to be a promising novel therapeutic to control sepsis [179], because rPPE18 significantly decreases the secretion of serum pro-inflammatory cytokines and reduces organ damage in mice infected with high doses of E. coli bacteria [179]
Summary
Animal cells rely on germline-encoded pattern recognition receptors (PRRs) to initiate protective innate immune responses [1,2]. PRRs recognize invading microbial pathogens through pathogen-associated molecular patterns (PAMPs) from the pathogens in combination with the recognition of danger-associated molecular patterns (DAMPs) produced by infected or damaged tissues [1,3,4]. PRRs can be divided into the following 8 wellcharacterized groups: Toll-like receptors (TLRs), retinoic acid-inducible gene-I (RIG)-I-like receptors (RLRs), nucleotide-binding oligomerization domain (NOD)-like receptors (NLRs), C-type lectin receptors (CLRs), opsonic receptors, AIM2-like receptors (ALRs), scavenger receptors (SRs), and stimulator of interferon genes (STING) [5,6,7]. PubMed. in Access to Pubmed theislink: https://pubmed.ncbi.nlm. The results ofThe theresults publication are sorted byexported “Year”. Of the counts publication countsand areexported sorted and by “Year”
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
