Abstract
Toll-like receptors (TLRs) represent a family of pattern recognition receptors that recognize certain pathogen-associated molecular patterns and damage-associated molecular patterns. TLRs are highly interesting to researchers including immunologists because of the involvement in various diseases including cancers, allergies, autoimmunity, infections, and inflammation. After ligand engagement, TLRs trigger multiple signaling pathways involving nuclear factor-κB (NF-κB), interferon-regulatory factors (IRFs), and mitogen-activated protein kinases (MAPKs) for the production of various cytokines that play an important role in diseases like cancer. TLR activation in immune as well as cancer cells may prevent the formation and growth of a tumor. Nonetheless, under certain conditions, either hyperactivation or hypoactivation of TLRs supports the survival and metastasis of a tumor. Therefore, the design of TLR-targeting agonists as well as antagonists is a promising immunotherapeutic approach to cancer. In this review, we mainly describe TLRs, their involvement in cancer, and their promising properties for anticancer drug discovery.
Highlights
Toll-like receptors (TLRs) belong to the family of pathogen recognition receptors (PRRs) in the innate immune system and recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) related to foreign invading pathogens and host cells, respectively
Thorough analysis has revealed that TLR4 mRNA is expressed by the Th17 subset of murine CD4+ T cells and that LPS stimulation increases the level of IL-17A and reduces that of IFNγ because of decreased activation of mitogen-activated protein kinases (MAPKs) [187,188]
The prime purpose of TLRs is to help the human body to develop immunity by activating various downstream signaling pathways that result in the secretion of diverse proinflammatory cytokines
Summary
Toll-like receptors (TLRs) belong to the family of pathogen recognition receptors (PRRs) in the innate immune system and recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs) related to foreign invading pathogens and host cells, respectively. Legend: AP-1, activated protein 1; BAX, BCL2-associated X; BCL, B-cell lymphoma protein; CDK, cyclin-dependent kinase; cIAP, cellular inhibitor of apoptosis protein; COX, cyclooxygenase; CSF, colony-stimulating factor; CXCL, chemokine (C-X-C motif) ligand; DAXX, death domain–associated protein; DR, death receptor; ELAM, endothelial-leukocyte adhesion molecule; ERK, extracellular signal–regulated kinase; FLIP, FLICE-like inhibitory protein; HIF, hypoxia-inducible factor; ICAM, intercellular adhesion molecule; IFN, interferon; IL, interleukin; iNOS, inducible NO synthase; IRF, interferon response factor; JNK, c-Jun N-terminal kinase; KAL, Kallmann syndrome gene; MAPK, mitogen-activated protein kinase; MCP, monocyte chemoattractant protein; MMP, matrix metalloproteinase; MnSOD, manganese superoxide dismutase; MyD88, myeloid differentiation primary response 88; NF-κB, nuclear factor κB; p38, protein 38; PML, promyelocytic leukemia protein; PUMA, p53-upregulated modulator of apoptosis; STAT, signal transducer and activator of transcription; TLR, Toll-like receptor; TNF-α, tumor necrosis factor α; TRAF, tumor necrosis factor receptor (TNF-R)-associated factor; uPA, urokinase-type plasminogen activator; VCAM, vascular cell adhesion molecule; VEGF, vascular endothelial growth factor; WAF, wild-type activating fragment; XIAP, x-linked inhibitor of apoptosis protein
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
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 callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
