Abstract
Innate immunity represents the first barrier for host defense against microbial infection. Toll-like receptors (TLRs) are the most well-defined PRRs with respect to PAMP recognition and induction of innate immune responses. They recognize pathogen-associated molecular patterns (PAMPs) and trigger innate immune responses by inducing inflammatory cytokines, chemokines, antigen-presenting molecules, and costimulatory molecules. TLRs are expressed either on the cell surface or within endosomes of innate immune cells. NK cells are one of the innate immune cells and also express TLRs to recognize or respond to PAMPs. TLRs in NK cells induce the innate immune responses against bacterial and viral infections via inducing NK cytotoxicity and cytokine production. In this review, we will discuss the expression and cellular function of TLRs in NK cells and also introduce some therapeutic applications of TLR agonists for NK cell-mediated immunotherapy.
Highlights
Cells involved in the innate immune response were initially speculated to nonspecifically eliminate microbes without presensitization; studies have reported that innate immune cells recognize microbial-associated or pathogen-associated molecular patterns (PAMPs) through their pattern recognition receptors (PRRs) including Tolllike receptors (TLRs), NOD-like receptors (NLRs), C-type lectin receptors (CLRs), and RIG-I-like receptors (RLRs) [1,2,3]
natural killer (NK) cells play an important role in the host response against various pathogens
TLRs are expressed on innate immune cells or some adaptive immune cells and mediate innate immune responses against microbial pathogens and induce adaptive immune responses
Summary
Cells involved in the innate immune response were initially speculated to nonspecifically eliminate microbes without presensitization; studies have reported that innate immune cells recognize microbial-associated or pathogen-associated molecular patterns (PAMPs) through their pattern recognition receptors (PRRs) including Tolllike receptors (TLRs), NOD-like receptors (NLRs), C-type lectin receptors (CLRs), and RIG-I-like receptors (RLRs) [1,2,3]. TLR expression and function in NK cells were revealed owing to their potential involvement in the Journal of Immunology Research innate immune response to bacterial and viral infections via induction of NK cell-mediated cytotoxicity and cytokine production [6, 8, 11, 12]. All TLRs induce the myeloid differentiation primary response protein 88- (MyD88-) dependent pathways except TLR3 [20] These sensors, TLRs, are differentially expressed among immune cells and have distinct functions in terms of PAMP recognition and immune responses. TLR3 was previously reported to recognize doublestranded RNA (dsRNA) produced by numerous viruses during replication or a synthetic analog of dsRNA, polyinosinicpolycytidylic acid (poly(I:C)), which mimics viral infection and induces antiviral immune responses by inducing type I interferons (IFNs) and inflammatory cytokines through the interaction of its ectodomain with dsRNA [23,24,25]. PAMP recognition by TLRs triggers intracellular signaling pathways to produce inflammatory cytokines, type I IFNs, and chemokines for innate immune responses (Figure 1)
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