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Academic literature on the topic 'AIM2-like receptors'
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Journal articles on the topic "AIM2-like receptors"
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Brunette, Rebecca L., Janet M. Young, Deborah G. Whitley, Igor E. Brodsky, Harmit S. Malik, and Daniel B. Stetson. "Extensive evolutionary and functional diversity among mammalian AIM2-like receptors." Journal of Experimental Medicine 209, no. 11 (October 8, 2012): 1969–83. http://dx.doi.org/10.1084/jem.20121960.
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Innate immune detection of nucleic acids is important for initiation of antiviral responses. Detection of intracellular DNA activates STING-dependent type I interferons (IFNs) and the ASC-dependent inflammasome. Certain members of the AIM2-like receptor (ALR) gene family contribute to each of these pathways, but most ALRs remain uncharacterized. Here, we identify five novel murine ALRs and perform a phylogenetic analysis of mammalian ALRs, revealing a remarkable diversification of these receptors among mammals. We characterize the expression, localization, and functions of the murine and human ALRs and identify novel activators of STING-dependent IFNs and the ASC-dependent inflammasome. These findings validate ALRs as key activators of the antiviral response and provide an evolutionary and functional framework for understanding their roles in innate immunity.
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Silva, Grace, Natália Carneiro, Dario Zamboni, and João Silva. "NLRP3 and AIM2 mediate nitric oxide production and macrophage resistance to T. cruzi infection (INM3P.442)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 57.5. http://dx.doi.org/10.4049/jimmunol.192.supp.57.5.
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Abstract The Toll-like receptors (TLRs), 2, 4 and 9 are important to immunity against Trypanosoma cruzi, etiologic agent of Chagas disease. Intracellular receptors, including NLRP3 and AIM2, associate to ASC forming a complex that active caspase-1, called inflammasome. This complex is required for cleavage of the active forms of the IL-1β and IL-18. Recently, we show that ASC inflammasome is necessary to control T. cruzi infection, however the receptors that participate in this signalizing are not complete clear. Here, we investigated the participation of NLRP3 and AIM2 in the immune response against T. cruzi. First, we found high IL-1β production and caspase-1 activation in BMMs from WT mice, but not from NLRP3-/- and AIM2-/- mice. To understand the role of the inflammasome pathway during T. cruzi infection, WT, caspase-1-/-, ASC-/-, AIM2-/- and NLRP3-/- mice were infected with Y strain of T.cruzi. Our results showed that ASC-/- and caspase-1-/- mice presented higher mortality, whereas WT, AIM3-/- and NLRP3-/- are resistant to infection, suggesting more than one NLR is necessary to confer resistance for T. cruzi infection. In addition, caspase-1-/-, ASC-/-, AIM2-/- and NLRP3 BMMs presented higher parasitism and reduced amount of Nitric oxide (NO) production. Together, these results suggest that AIM2 and NLRP3 via ASC inflammasome participate of the infection against T. cruzi. Financial Support: FAPESP
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Jiang, Hui, Patrycja Swacha, and Nelson O. Gekara. "Nuclear AIM2‐Like Receptors Drive Genotoxic Tissue Injury by Inhibiting DNA Repair." Advanced Science 8, no. 22 (October 18, 2021): 2102534. http://dx.doi.org/10.1002/advs.202102534.
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Gray, Elizabeth E., Damion Winship, Jessica M. Snyder, Stephanie J. Child, Adam P. Geballe, and Daniel B. Stetson. "The AIM2-like Receptors Are Dispensable for the Interferon Response to Intracellular DNA." Immunity 45, no. 2 (August 2016): 255–66. http://dx.doi.org/10.1016/j.immuni.2016.06.015.
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Gray, Elizabeth, and Daniel B. Stetson. "The AIM2-like receptors are dispensable for activation of the interferon stimulatory DNA (ISD) pathway." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 203.10. http://dx.doi.org/10.4049/jimmunol.196.supp.203.10.
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Abstract Detection of intracellular DNA triggers activation of the STING-dependent interferon-stimulatory DNA (ISD) pathway, which is essential for antiviral immune responses; on the other hand, inappropriate immune responses to self DNA result in autoimmunity. Multiple DNA sensors have been proposed to activate the ISD pathway, including cyclic GMP-AMP synthase (cGAS) and a family of DNA binding receptors called the AIM2-like receptors (ALRs). Analysis of cGAS-deficient mice has revealed that cGAS is a key DNA sensor that is required for activation of the ISD pathway; however, whether the ALRs contribute to this pathway remains unclear. Here, we generated mice lacking all 13 mouse ALR genes as a novel tool to explore the function of the ALRs. We show that all ALRs are dispensable for the type I interferon (IFN) response to transfected DNA ligands, DNA virus infection, and lentivirus infection. We also show that the DNA sensor cGAS, but not the ALRs, is required to drive autoimmune disease in the Trex1-deficient mouse model of Aicardi-Goutieres Syndrome. Finally, we used CRISPR to disrupt the human AIM2-like receptor IFI16 in primary human fibroblasts and show that IFI16 is dispensable for the IFN response to transfected DNA ligands as well as human cytomegalovirus (HCMV) infection. Thus, our data reveal that ALRs are dispensable for activation of the ISD pathway and demonstrate that cGAS is the primary DNA sensor that drives the IFN response to DNA.
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Jang, Ji-Hyun, Hee Woong Shin, Jung Min Lee, Hyeon-Woo Lee, Eun-Cheol Kim, and Sang Hyuk Park. "An Overview of Pathogen Recognition Receptors for Innate Immunity in Dental Pulp." Mediators of Inflammation 2015 (2015): 1–12. http://dx.doi.org/10.1155/2015/794143.
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Pathogen recognition receptors (PRRs) are a class of germ line-encoded receptors that recognize pathogen-associated molecular patterns (PAMPs). The activation of PRRs is crucial for the initiation of innate immunity, which plays a key role in first-line defense until more specific adaptive immunity is developed. PRRs differ in the signaling cascades and host responses activated by their engagement and in their tissue distribution. Currently identified PRR families are the Toll-like receptors (TLRs), the C-type lectin receptors (CLRs), the nucleotide-binding oligomerization domain-like receptors (NLRs), the retinoic acid-inducible gene-I-like receptors (RLRs), and the AIM2-like receptor (ALR). The environment of the dental pulp is substantially different from that of other tissues of the body. Dental pulp resides in a low compliance root canal system that limits the expansion of pulpal tissues during inflammatory processes. An understanding of the PRRs in dental pulp is important for immunomodulation and hence for developing therapeutic targets in the field of endodontics. Here we comprehensively review recent finding on the PRRs and the mechanisms by which innate immunity is activated. We focus on the PRRs expressed on dental pulp and periapical tissues and their role in dental pulp inflammation.
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Wang, Li-Jie, Chia-Wei Hsu, Chiu-Chin Chen, Ying Liang, Lih-Chyang Chen, David M. Ojcius, Ngan-Ming Tsang, Chuen Hsueh, Chih-Ching Wu, and Yu-Sun Chang. "Interactome-wide Analysis Identifies End-binding Protein 1 as a Crucial Component for the Speck-like Particle Formation of Activated Absence in Melanoma 2 (AIM2) Inflammasomes." Molecular & Cellular Proteomics 11, no. 11 (August 6, 2012): 1230–44. http://dx.doi.org/10.1074/mcp.m112.020594.
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Inflammasomes are cytoplasmic receptors that can recognize intracellular pathogens or danger signals and are critical for interleukin 1β production. Although several key components of inflammasome activation have been identified, there has not been a systematic analysis of the protein components found in the stimulated complex. In this study, we used the isobaric tags for relative and absolute quantification approach to systemically analyze the interactomes of the NLRP3, AIM2, and RIG-I inflammasomes in nasopharyngeal carcinoma cells treated with specific stimuli of these interactomes (H2O2, poly (dA:dT), and EBV noncoding RNA, respectively). We identified a number of proteins that appeared to be involved in the interactomes and also could be precipitated with anti-apoptosis-associated speck-like protein containing caspase activation and recruitment domain antibodies after stimulation. Among them, end binding protein 1 was an interacting component in all three interactomes. Silencing of end binding protein 1 expression by small interfering RNA inhibited the activation of the three inflammasomes, as indicated by reduced levels of interleukin 1β secretion. We confirmed that end binding protein 1 directly interacted with AIM2 and ASC in vitro and in vivo. Most importantly, fluorescence confocal microscopy showed that end binding protein 1 was required for formation of the speck-like particles that represent activation of the AIM2 inflammasome. In nasopharyngeal carcinoma tissues, immunohistochemical staining showed that end binding protein 1 expression was elevated and significantly correlated with AIM2 and ASC expression in nasopharyngeal carcinoma tumor cells. In sum, we profiled the interactome components of three inflammasomes and show for the first time that end binding protein 1 is crucial for the speck-like particle formation that represents activated inflammasomes.
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Lu, Jianlin, Jessica M. Gullett, and Thirumala-Devi Kanneganti. "Filoviruses: Innate Immunity, Inflammatory Cell Death, and Cytokines." Pathogens 11, no. 12 (November 23, 2022): 1400. http://dx.doi.org/10.3390/pathogens11121400.
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Filoviruses are a group of single-stranded negative sense RNA viruses. The most well-known filoviruses that affect humans are ebolaviruses and marburgviruses. During infection, they can cause life-threatening symptoms such as inflammation, tissue damage, and hemorrhagic fever, with case fatality rates as high as 90%. The innate immune system is the first line of defense against pathogenic insults such as filoviruses. Pattern recognition receptors (PRRs), including toll-like receptors, retinoic acid-inducible gene-I-like receptors, C-type lectin receptors, AIM2-like receptors, and NOD-like receptors, detect pathogens and activate downstream signaling to induce the production of proinflammatory cytokines and interferons, alert the surrounding cells to the threat, and clear infected and damaged cells through innate immune cell death. However, filoviruses can modulate the host inflammatory response and innate immune cell death, causing an aberrant immune reaction. Here, we discuss how the innate immune system senses invading filoviruses and how these deadly pathogens interfere with the immune response. Furthermore, we highlight the experimental difficulties of studying filoviruses as well as the current state of filovirus-targeting therapeutics.
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Latz, Eicke. "New Insights into the Biology of Toll-Like Receptors and Inflammasomes." Blood 114, no. 22 (November 20, 2009): SCI—23—SCI—23. http://dx.doi.org/10.1182/blood.v114.22.sci-23.sci-23.
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Abstract Abstract SCI-23 Innate immunity evolved to recognize microbial infection and to respond to danger signals that appear under disease conditions. The most recently described innate immune receptor family is the Nod-like receptor (NLR) family. The inflammatory cytokines IL-1b and IL-18 are released only upon cleavage by the inflammatory caspase-1. Caspase-1 activity itself is controlled by a cytosolic signaling complex consisting of the NLR member NALP3 and the adapter protein ASC. After activation NALP3, ASC and caspase-1 form a multi-molecular complex termed the NALP3 inflammasome. The NALP3 inflammasome is activated in response to various membrane active bacterial toxins (e.g. nigericin, maitotoxin or gramicidin) or by incubation with crystalline materials (e.g. silica, asbestos, monosodium urate or alum). The mechanisms by which the NALP3 inflammasome is activated by physico-chemical diverse activators are not well understood. We demonstrate that crystals activate the NALP3 inflammasome in a process that requires phagocytosis and crystal uptake leads to lysosomal damage and rupture. Furthermore, sterile lysosomal damage is also sufficient to induce NALP3 activation and inhibition of phagosomal acidification or inhibition or lack of cathepsins impairs NALP3 activation. These results indicate that the NALP3 inflammasome can sense lysosomal damage induced by various means as an endogenous danger signal. Our results demonstrate a novel strategy of immune cells to recognize different classes of stimuli by a common, indirect mechanism. Cytosolic DNA can activate a NALP3 independent yet ASC dependent inflammasome. AIM2, a member of the PYHIN protein family, has a pyrin domain and a HIN200 DNA binding domain. We discovered that AIM2 binds to dsDNA and forms an inflammasome with ASC leading to caspase 1 activation. These pathways are promising new targets for pharmacological inhibitors with broad clinical significance. Disclosures No relevant conflicts of interest to declare.
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Chou, Wei-Chun, Elena Rampanelli, Xin Li, and Jenny P. Y. Ting. "Impact of intracellular innate immune receptors on immunometabolism." Cellular & Molecular Immunology 19, no. 3 (October 25, 2021): 337–51. http://dx.doi.org/10.1038/s41423-021-00780-y.
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AbstractImmunometabolism, which is the metabolic reprogramming of anaerobic glycolysis, oxidative phosphorylation, and metabolite synthesis upon immune cell activation, has gained importance as a regulator of the homeostasis, activation, proliferation, and differentiation of innate and adaptive immune cell subsets that function as key factors in immunity. Metabolic changes in epithelial and other stromal cells in response to different stimulatory signals are also crucial in infection, inflammation, cancer, autoimmune diseases, and metabolic disorders. The crosstalk between the PI3K–AKT–mTOR and LKB1–AMPK signaling pathways is critical for modulating both immune and nonimmune cell metabolism. The bidirectional interaction between immune cells and metabolism is a topic of intense study. Toll-like receptors (TLRs), cytokine receptors, and T and B cell receptors have been shown to activate multiple downstream metabolic pathways. However, how intracellular innate immune sensors/receptors intersect with metabolic pathways is less well understood. The goal of this review is to examine the link between immunometabolism and the functions of several intracellular innate immune sensors or receptors, such as nucleotide-binding and leucine-rich repeat-containing receptors (NLRs, or NOD-like receptors), absent in melanoma 2 (AIM2)-like receptors (ALRs), and the cyclic dinucleotide receptor stimulator of interferon genes (STING). We will focus on recent advances and describe the impact of these intracellular innate immune receptors on multiple metabolic pathways. Whenever appropriate, this review will provide a brief contextual connection to pathogenic infections, autoimmune diseases, cancers, metabolic disorders, and/or inflammatory bowel diseases.
Dissertations / Theses on the topic "AIM2-like receptors"
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Ghosh, Sreya. "Different Journeys, Same Destination: Exploring the Role of a PYHIN Protein and Involvement of Caspase-8 in the Regulation and Activation of Inflammasomes." eScholarship@UMMS, 2009. http://escholarship.umassmed.edu/gsbs_diss/928.
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Interferon-inducible PYHIN protein family includes the DNA-binding proteins, AIM2 and IFI16, which form ASC-caspase 1 dependent inflammasomes, important in immunity against cytosolic bacteria, DNA viruses and HIV. The role of other members of this family in the recognition of DNA and/or regulation of immune responses is unclear. We identified an immune regulatory function of p205, another member of the PYHIN family, in the transcriptional control of immune genes. Knockdown of p205 in macrophages revealed that inflammasome activation due to dsDNA and ligands that engage the NLRP3 inflammasome were severely compromised. Detailed mechanistic analysis showed that loss of p205 was associated with a decrease in Asc mRNA and protein levels. p205 knockdown resulted in reduced RNA Polymerase II-mediated endogenous Asc gene transcription and mRNA processing, suggesting a co-transcriptional control of Asc gene expression. Ectopically expressed p205 induced expression of an Asc gene-luciferase reporter and collaborated with other transcription factors, such as c/EBPβ, p65/RelA, to further enhance expression. p205 knockdown also affected the expression of the immune genes Cd86, Cox2, Cxcl2, Il1α, Il10, Il12α, Il6 and Ifnα in LPS-stimulated macrophages. Together these findings suggest that p205 regulates inflammation through control of Asc gene expression, and other immune genes.
Fungal infections activate both caspase 1-dependent and -independent inflammasomes. In an independent study, we show that Paracoccidioides brasiliensis fungal infection also induces caspase 8-dependent non-canonical inflammasome. Caspase 8-dependent IL-1β processing required dectin-1, Syk and Asc. Rip3-/- Casp8-/- mice infected with P. brasiliensis displayed increased fungal load and showed worse disease progression compared to wild type and Rip3-/- mice. These results revealed the importance of caspase 8 in activating and regulating inflammasome responses during fungal infection in vivo.
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Ghosh, Sreya. "Different Journeys, Same Destination: Exploring the Role of a PYHIN Protein and Involvement of Caspase-8 in the Regulation and Activation of Inflammasomes." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/928.
Full textAbstract:
Interferon-inducible PYHIN protein family includes the DNA-binding proteins, AIM2 and IFI16, which form ASC-caspase 1 dependent inflammasomes, important in immunity against cytosolic bacteria, DNA viruses and HIV. The role of other members of this family in the recognition of DNA and/or regulation of immune responses is unclear. We identified an immune regulatory function of p205, another member of the PYHIN family, in the transcriptional control of immune genes. Knockdown of p205 in macrophages revealed that inflammasome activation due to dsDNA and ligands that engage the NLRP3 inflammasome were severely compromised. Detailed mechanistic analysis showed that loss of p205 was associated with a decrease in Asc mRNA and protein levels. p205 knockdown resulted in reduced RNA Polymerase II-mediated endogenous Asc gene transcription and mRNA processing, suggesting a co-transcriptional control of Asc gene expression. Ectopically expressed p205 induced expression of an Asc gene-luciferase reporter and collaborated with other transcription factors, such as c/EBPβ, p65/RelA, to further enhance expression. p205 knockdown also affected the expression of the immune genes Cd86, Cox2, Cxcl2, Il1α, Il10, Il12α, Il6 and Ifnα in LPS-stimulated macrophages. Together these findings suggest that p205 regulates inflammation through control of Asc gene expression, and other immune genes.
Fungal infections activate both caspase 1-dependent and -independent inflammasomes. In an independent study, we show that Paracoccidioides brasiliensis fungal infection also induces caspase 8-dependent non-canonical inflammasome. Caspase 8-dependent IL-1β processing required dectin-1, Syk and Asc. Rip3-/- Casp8-/- mice infected with P. brasiliensis displayed increased fungal load and showed worse disease progression compared to wild type and Rip3-/- mice. These results revealed the importance of caspase 8 in activating and regulating inflammasome responses during fungal infection in vivo.