TLR ligands are present on both commensal and pathogenic microbes. Intestinal epithelial cells (IECs) have been observed to be largely unresponsive to TLR ligands. This observation has partly been explained by the fact that TLR expression on IECs is sparse. The discovery of the Toll-like receptors finally identified the innate immune receptors that were responsible for many of the innate immune functions that had been studied for many years. Interestingly, TLRs seem only to be involved in the cytokine production and cellular activation in response to microbes, and do not play a significant role in the adhesion and phagocytosis of microorganisms. One member of this group, interleukin-1β (IL-1β), together with tumour-necrosis factor (TNF), is defined as an ‘alarm cytokine’. It is secreted by macrophages and initiates inflammation on activation of TLRs.
Toll-like receptors, inflammation, commensal bacteria, cytokine, TLRs, TLR ligands, tumour-necrosis factor (TNF), alarm cytokine, expression of TLR, MyD88-Dependent Signaling, MyD88-Independent Signaling, TLR Signaling Pathways, Various Type of TLRs, Commensal Bacteria and TLR
Department of Bacteriology and Research Center of Microbiology, Pasteur Institute of Iran, Tehran,Iran.