Innate immunity not only represents the first line of defence against invading microbial pathogens but also is the first step towards the activation and stimulation of adaptive immunity. Upon exposure to bacteria, viruses, protozoa and fungi, innate immune cells including neutrophils, monocytes, macrophages, dendritic cells (DCs), natural killer (NK) cells and the complement system are activated. The response of the innate immunity to microbial pathogens relies on the specific host-receptor detection of pathogen-and danger-derived molecular signatures, known as PAMPs and DAMPs, respectively. When PAMPs and DAMPs are recognized by germline-encoded pattern-recognition receptors (PRRs), different types of cytokines would be released, which in turn attract secondary defensive immune cells. In the long list of PRRs, Tolllike receptors (TLRs) are the most important ones. TLRs are one of the largest and most well-studied families of PRRs, which were first recognized in the fruit fly, Drosophila melanogaster. 1 Not only these receptors are one of the main components of innate immunity, infection diseases, and inflammatory conditions, but also they act as a bridge between innate and adaptive immunity. Apart from regulatory role in immune responses, TLRs have a hand in tissue homeostasis maintenance by regulating tissue repair and regeneration. But the mystery behind TLR functions in the cells was not limited only to these findings, and there was some evidence supporting the fact that they might have