Pathogen Recognition by the Innate Immune System
By Himanshu Kumar, Taro Kawai, Shizuo Akira. International Reviews of Immunology, 2011
2,192 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/75985da9cdcc6adf12edfcc2693ecec68c869c8d
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In Immunology
In Molecular Biology
Citations in the corpus
- Vaccine instability in the cold chain: mechanisms, analysis and formulation strategies. (2014, background): “The innate immune system possesses receptors that have evolved to recognize the patterns of such molecules [13,14].”
- Exosomes and other extracellular vesicles in host–pathogen interactions (2014, positive): “The importance of PRRs in the recognition and response to pathogens has been shown in both animal infection models and human studies [1].”
- Inflammation and its role in age-related macular degeneration (2016, background): “The ligand recognition process triggers the activation of intracellular signaling pathways resulting in the production of numerous pro-inflammatory mediators [34].”
- NF-κB signaling in inflammation (2017, neutral): “18,20,21 The different families of PRRs have distinct structural properties and respond to different PAMPs and DAMPs, but they share many similarities in the downstream signal transduction pathways.”
- Pathogenicity and virulence of Staphylococcus aureus (2021, background): “and usually activate Toll-like receptors (TLRs) [57], which function as homo- or heterodimers.”
- The crucial roles of inflammatory mediators in inflammation: A review (2018, background): “The mechanism of phagocytosis needs the employment of actin filaments during internalization response [98].”
- DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote anti-microbial innate immunity. (2015, background): “Type I interferons (IFNs), the main effector cytokines against viral infections, are inducedmainly via the activation of pattern-recognition receptors (PRRs) such as Toll-like receptors (TLRs), RIG-Ilike receptors (RLRs), and the newly identified STING-dependent pathways that recognize microbial and”
- Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL* (2013, background): “TLRs, like TNF family death receptors, mediate cytokine and interferon activation (3), while also hold-”