The family of Toll-like receptors (TLR1-TLR11) provides host defense in mammals by inducing proinflammatory innate immune response upon recognition of conserved structural component in pathogens. TLR mediated activation of signaling pathways that induce the expression of proinflammatory molecules is one of the well-studied but ever expanding fields of immunology. As a result, a wealth of information has been obtained which includes the identification of specific ligands of individual TLR, elucidation of their downstream signaling pathways, function of different adaptor proteins, activation of protein kinases and transcription factors that transcribe the genes for inflammatory molecules. TLRs not only sense microbial invasion but also can be activated by endogenous molecules as well as low molecular weight synthetic compounds. Given the role of innate immune machinery to provoke inflammation in host, TLRs signaling may be involved in many acute and chronic inflammatory processes in sterile and post-infection conditions such as, atherosclerosis, leprosy, inflammatory bowel syndrome (IBD), lung airway hyperactivity in allergic asthma, and in sepsis. By the same token, TLRs can also be associated with autoimmune diseases such as systemic lupus erythematosus (SLE) or other immune unresponsive diseases like cancer. In addition, synthetic organic compounds which enhance the function of TLRs can also be useful as potential adjutants to improve conventional vaccination strategy. Here we summarize the recent development on possible modulation of the TLR signaling pathway for therapeutic solution of multiple immune-related diseases.
Keywords: toll like receptors, agonist-antagonist, inflammation, allergic asthma, cancer, atherosclerosis and vaccine
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