title: NOD-Like Receptors in Infection, Immunity, and Diseases.
abstract: Nucleotide-binding and oligomerization domain (NOD)-like receptors (NLRs) are pattern-recognition receptors similar to toll-like receptors (TLRs). While TLRs are transmembrane receptors, NLRs are cytoplasmic receptors that play a crucial role in the innate immune response by recognizing pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs). Based on their N-terminal domain, NLRs are divided into four subfamilies: NLRA, NLRB, NLRC, and NLRP. NLRs can also be divided into four broad functional categories: inflammasome assembly, signaling transduction, transcription activation, and autophagy. In addition to recognizing PAMPs and DAMPs, NLRs act as a key regulator of apoptosis and early development. Therefore, there are significant associations between NLRs and various diseases related to infection and immunity. NLR studies have recently begun to unveil the roles of NLRs in diseases such as gout, cryopyrin-associated periodic fever syndromes, and Crohn's disease. As these new associations between NRLs and diseases may improve our understanding of disease pathogenesis and lead to new approaches for the prevention and treatment of such diseases, NLRs are becoming increasingly relevant to clinicians. In this review, we provide a concise overview of NLRs and their role in infection, immunity, and disease, particularly from clinical perspectives.
authors.affiliation: Department of Internal Medicine, Yonsei University Wonju College of Medicine, Wonju, Korea.
authors.forename: Young Keun
authors.initials: YK
authors.lastname: Kim
authors.affiliation: Department of Microbiology, Yonsei University College of Medicine, Seoul, Korea.|Brain Korea 21 PLUS for Medical Science, Yonsei University College of Medicine, Seoul, Korea.|Severance Biomedical Science Institute and Institute for Immunology and Immunological Diseases, Yonsei University College of Medicine, Seoul, Korea.
authors.forename: Jeon Soo
authors.initials: JS
authors.lastname: Shin
authors.affiliation: Department of Pathology, University of Alabama at Birmingham, Birmingham, AL, USA. nahm@uab.edu.|Department of Microbiology, University of Alabama at Birmingham, Birmingham, AL, USA.
authors.forename: Moon H
authors.initials: MH
authors.lastname: Nahm
mesh_terms: D001343:Autophagy / Q000276:immunology; D002352:Carrier Proteins; D006801:Humans; D007113:Immunity, Innate; D058847:Inflammasomes; D053472:Nod Signaling Adaptor Proteins / Q000276:immunology / Q000378:metabolism*; D000069452:Pathogen-Associated Molecular Pattern Molecules; D018160:Receptors, Cytoplasmic and Nuclear / Q000276:immunology / Q000378:metabolism*; D051192:Receptors, Pattern Recognition / Q000276:immunology*; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000378:metabolism
chemical_list: D002352:Carrier Proteins; D058847:Inflammasomes; D053472:Nod Signaling Adaptor Proteins; D000069452:Pathogen-Associated Molecular Pattern Molecules; D018160:Receptors, Cytoplasmic and Nuclear; D051192:Receptors, Pattern Recognition; D051193:Toll-Like Receptors
keywords: Innate immunity; NOD-like receptors; inflammasomes; pattern recognition receptors