Abstract
Toll-like receptors (TLRs) are the important mediators of inflammatory pathways in the gut which play a major role in mediating the immune responses towards a wide variety of pathogen-derived ligands and link adaptive immunity with the innate immunity. Numerous studies in different populations across the continents have reported on the significant roles of TLR gene polymorphisms in modulating the risk of colorectal cancer (CRC). CRC is one of the major malignancies affecting the worldwide population and is currently ranking the third most common cancer in the world. In this review, we have attempted to discuss the structure, functions, and signaling of TLRs in comprehensive detail together with the role played by various TLR gene SNPs in CRC susceptibility.
Highlights
Colorectal cancer (CRC) is one of the commonly diagnosed cancers representing about 10% of all cancers worldwide and is currently ranked as the third most common cancer in men and second most in women worldwide [1,2,3]
As inflammation is considered as the important risk factor for the colorectal cancer (CRC) and Toll-like receptors (TLRs) playing a central role in inflammationdriven immune responses, TLRs have a universal role in carcinogenesis mechanism
Numerous TLRs 2, 3, 4, 7, 8, and 9 have been identified as molecules of interest for the development of agonist, antagonist, and vaccines to develop a treatment strategy to control and prevent the development of CRC, which has a heavy bearing upon the TLR gene SNPs and the effects they have on immune modulation
Summary
Colorectal cancer (CRC) is one of the commonly diagnosed cancers representing about 10% of all cancers worldwide and is currently ranked as the third most common cancer in men and second most in women worldwide [1,2,3]. Toll-like receptors (TLRs) are evolutionarily conserved receptors belonging to the family of pattern recognition receptors (PRRs) which play a vital role in immune responses especially pathogen recognition by the extracellular matrix [18, 29,30,31]. PRR signaling leads to the triggering of various processes involved in autophagy, cell death, cytokine processing, and phagocytosis [40, 41] Based on their composition and structure, PRRs are categorized into five classes depending on their primary functions, position, specificity for ligands, and evolutionary associations as follows:. V-Type TLRs possess a single cluster of cysteine or CF motif on their CTDs (LRRCT) and referred to as Single Cysteine Cluster TLRs (sccTLRs), and P-Type TLRs have multiple (two or more) cysteine clusters or CF motifs either on their LRRCT or on the N-terminal (LRRNT) domain [54, 55]
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