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Article: Association of Endocrine Therapy and Dementia in Women with Breast Cancer.

Thompson, Mikayla R / Niu, Jiangong / Lei, Xiudong / Nowakowska, Malgorzata / Wehner, Mackenzie R / Giordano, Sharon H / Nead, Kevin T

Breast cancer (Dove Medical Press)

2021 Volume 13, Page(s) 219–224

Abstract: Purpose: Prior studies have reported differing results regarding the association between endocrine therapy (ET) in the treatment of breast cancer and dementia risk. However, existing findings may be limited by common sources of bias and confounding. ... ...

Abstract	Purpose: Prior studies have reported differing results regarding the association between endocrine therapy (ET) in the treatment of breast cancer and dementia risk. However, existing findings may be limited by common sources of bias and confounding. Here we investigate the association of ET utilized in the definitive setting to treat non-metastatic breast cancer with dementia risk accounting for multiple potential sources of bias and confounding. Patients and methods: We conducted a retrospective study in SEER-Medicare of women aged ≥ 66 years with non-metastatic breast cancer. We examined the risk of all-cause dementia among ET users versus non-ET users using multivariable regression models, accounting for the competing risk of death, and using a start of the follow-up period as 12-months following breast cancer diagnosis for both groups to avoid immortal time bias. Results: Among 25,777 individuals there were 2,869 incident dementia cases. We found a statistically significantly decreased risk of any dementia among ET users in unadjusted and adjusted models that completely attenuated when accounting for the competing risk of death (hazard ratio, 0.98; 95% confidence interval, 0.90-1.07). Conclusion: When accounting for common sources of bias and confounding we did not find evidence to support an association between ET in the definitive treatment of non-metastatic breast cancer and dementia risk. These results suggest that ET may not be associated with dementia risk.
Language	English
Publishing date	2021-04-07
Publishing country	New Zealand
Document type	Journal Article
ZDB-ID	2520722-2
ISSN	1179-1314
ISSN	1179-1314
DOI	10.2147/BCTT.S300455
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Article ; Online: Association of statin use with clinical outcomes in patients with triple-negative breast cancer.

Nowakowska, Malgorzata K / Lei, Xiudong / Thompson, Mikayla T / Shaitelman, Simona F / Wehner, Mackenzie R / Woodward, Wendy A / Giordano, Sharon H / Nead, Kevin T

Cancer

2021 Volume 127, Issue 22, Page(s) 4142–4150

Abstract: Background: Previous studies have examined the association of statin therapy and breast cancer outcomes with mixed results. The objective of this study was to investigate the clinical effects of incident statin use among individuals with triple-negative ...

Abstract	Background: Previous studies have examined the association of statin therapy and breast cancer outcomes with mixed results. The objective of this study was to investigate the clinical effects of incident statin use among individuals with triple-negative breast cancer (TNBC). Methods: Data from the Surveillance, Epidemiology, and End Results-Medicare and Texas Cancer Registry-Medicare databases were used, and women aged ≥66 years who had stage I, II, and III breast cancer were identified. Multivariable Cox proportional hazards regression models were used to examine the association of new statin use in the 12 months after a breast cancer diagnosis with overall survival (OS) and breast cancer-specific survival (BCSS). Results: When examining incident statin use, defined as the initiation of statin therapy in the 12 months after breast cancer diagnosis, a significant association was observed between statin use and improved BCSS (standardized hazard ratio, 0.42; 95% confidence interval [CI], 0.20-0.88; P = .022) and OS (hazard ratio, 0.70; 95% CI, 0.50-0.99; P = .046) among patients with TNBC (n = 1534). No association was observed with BCSS (standardized hazard ratio, 0.99; 95% CI, 0.71-1.39; P = .97) or OS (hazard ratio, 1.04; 95% CI, 0.92-1.17; P = .55) among those without TNBC (n = 15,979). The results were consistent when examining statin exposure as a time-varying variable. Conclusions: Among women with I, II, and III TNBC, initiation of statin therapy in the 12 months after breast cancer diagnosis was associated with an OS and BCSS benefit. Statins may have a role in select patients with breast cancer, and further investigation is warranted.
MeSH term(s)	Aged ; Breast Neoplasms/drug therapy ; Breast Neoplasms/epidemiology ; Databases, Factual ; Female ; Humans ; Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use ; Medicare ; Proportional Hazards Models ; Triple Negative Breast Neoplasms/diagnosis ; Triple Negative Breast Neoplasms/drug therapy ; Triple Negative Breast Neoplasms/epidemiology ; United States/epidemiology
Chemical Substances	Hydroxymethylglutaryl-CoA Reductase Inhibitors
Language	English
Publishing date	2021-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1429-1
ISSN	1097-0142 ; 0008-543X ; 1934-662X
ISSN (online)	1097-0142
ISSN	0008-543X ; 1934-662X
DOI	10.1002/cncr.33797
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Article ; Online: Association of clonal hematopoiesis mutations with clinical outcomes: A systematic review and meta-analysis.

Nowakowska, Malgorzata K / Kim, Taebeom / Thompson, Mikayla T / Bolton, Kelly L / Deswal, Anita / Lin, Steven H / Scheet, Paul / Wehner, Mackenzie R / Nead, Kevin T

American journal of hematology

2022 Volume 97, Issue 4, Page(s) 411–420

Abstract: Clonal hematopoiesis (CH) mutations are common among individuals without known hematologic disease. CH mutations have been associated with numerous adverse clinical outcomes across many different studies. We systematically reviewed the available ... ...

Abstract	Clonal hematopoiesis (CH) mutations are common among individuals without known hematologic disease. CH mutations have been associated with numerous adverse clinical outcomes across many different studies. We systematically reviewed the available literature for clinical outcomes associated with CH mutations in patients without hematologic disease. We searched PubMed, EMBASE, and Scopus for eligible studies. Three investigators independently extracted the data, and each study was verified by a second author. Risk of bias was assessed using the Newcastle-Ottawa Scale. We identified 32 studies with 56 cohorts that examine the association between CH mutations and clinical outcomes. We conducted meta-analyses comparing outcomes among individuals with and without detectable CH mutations. We conducted meta-analyses for cardiovascular diseases (nine studies; HR = 1.61, 95% CI = 1.26-2.07, p = .0002), hematologic malignancies (seven studies; HR = 5.59, 95% CI = 3.31-9.45, p < .0001), therapy-related myeloid neoplasms (four studies; HR = 7.55, 95% CI = 4.3-13.57, p < .001), and death (nine studies; HR = 1.34, 95% CI = 1.2-1.5, p < .0001). The cardiovascular disease analysis was further stratified by variant allele fraction (VAF) and gene, which showed a statistically significant association only with a VAF of ≥ 10% (HR = 1.42, 95% CI = 1.24-1.62, p < .0001), as well as statistically significant associations for each gene examined with the largest magnitude of effect found for CH mutations in JAK2 (HR = 3.5, 95% CI = 1.84-6.68, p < .0001). Analysis of the association of CH mutations with hematologic malignancy demonstrated a numeric stepwise increase in risk with increasing VAF thresholds. This analysis strongly supports the association of CH mutations with a clinically meaningful increased risk of adverse clinical outcomes among individuals without hematologic disease, particularly with increasing VAF thresholds.
MeSH term(s)	Alleles ; Clonal Hematopoiesis/genetics ; Hematologic Neoplasms/genetics ; Hematologic Neoplasms/therapy ; Hematopoiesis/genetics ; Humans ; Mutation ; Neoplasms, Second Primary/genetics
Language	English
Publishing date	2022-01-19
Publishing country	United States
Document type	Journal Article ; Meta-Analysis ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Systematic Review
ZDB-ID	196767-8
ISSN	1096-8652 ; 0361-8609
ISSN (online)	1096-8652
ISSN	0361-8609
DOI	10.1002/ajh.26465
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Article ; Online: Pattern Recognition Receptors and the Innate Immune Response to Viral Infection

Katherine A. Fitzgerald / Evelyn A. Kurt-Jones / John J. Kaminski / Mikayla R. Thompson

Viruses, Vol 3, Iss 6, Pp 920-

2011 Volume 940

Abstract: The innate immune response to viral pathogens is critical in order to mobilize protective immunity. Cells of the innate immune system detect viral infection largely through germline-encoded pattern recognition receptors (PRRs) present either on the cell ... ...

Abstract	The innate immune response to viral pathogens is critical in order to mobilize protective immunity. Cells of the innate immune system detect viral infection largely through germline-encoded pattern recognition receptors (PRRs) present either on the cell surface or within distinct intracellular compartments. These include the Toll-like receptors (TLRs), the retinoic acid-inducble gene I-like receptors (RLRs), the nucleotide oligomerization domain-like receptors (NLRs, also called NACHT, LRR and PYD domain proteins) and cytosolic DNA sensors. While in certain cases viral proteins are the trigger of these receptors, the predominant viral activators are nucleic acids. The presence of viral sensing PRRs in multiple cellular compartments allows innate cells to recognize and quickly respond to a broad range of viruses, which replicate in different cellular compartments. Here, we review the role of PRRs and associated signaling pathways in detecting viral pathogens in order to evoke production of interferons and cytokines. By highlighting recent progress in these areas, we hope to convey a greater understanding of how viruses activate PRR signaling and how this interaction shapes the anti-viral immune response.
Keywords	pattern recognition receptor ; toll like receptor ; nod like receptor ; AIM2 like receptor ; RIG-I like receptor ; cytosolic DNA sensor ; inflammasome ; interferon ; virus ; Microbiology ; QR1-502 ; Science ; Q ; DOAJ:Microbiology ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Subject code	612
Language	English
Publishing date	2011-06-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Interferon γ-inducible protein (IFI) 16 transcriptionally regulates type i interferons and other interferon-stimulated genes and controls the interferon response to both DNA and RNA viruses.

Thompson, Mikayla R / Sharma, Shruti / Atianand, Maninjay / Jensen, Søren B / Carpenter, Susan / Knipe, David M / Fitzgerald, Katherine A / Kurt-Jones, Evelyn A

The Journal of biological chemistry

2014 Volume 289, Issue 34, Page(s) 23568–23581

Abstract: The interferon γ-inducible protein 16 (IFI16) has recently been linked to the detection of nuclear and cytosolic DNA during infection with herpes simplex virus-1 and HIV. IFI16 binds dsDNA via HIN200 domains and activates stimulator of interferon genes ( ... ...

Abstract	The interferon γ-inducible protein 16 (IFI16) has recently been linked to the detection of nuclear and cytosolic DNA during infection with herpes simplex virus-1 and HIV. IFI16 binds dsDNA via HIN200 domains and activates stimulator of interferon genes (STING), leading to TANK (TRAF family member-associated NF-κB activator)-binding kinase-1 (TBK1)-dependent phosphorylation of interferon regulatory factor (IRF) 3 and transcription of type I interferons (IFNs) and related genes. To better understand the role of IFI16 in coordinating type I IFN gene regulation, we generated cell lines with stable knockdown of IFI16 and examined responses to DNA and RNA viruses as well as cyclic dinucleotides. As expected, stable knockdown of IFI16 led to a severely attenuated type I IFN response to DNA ligands and viruses. In contrast, expression of the NF-κB-regulated cytokines IL-6 and IL-1β was unaffected in IFI16 knockdown cells, suggesting that the role of IFI16 in sensing these triggers was unique to the type I IFN pathway. Surprisingly, we also found that knockdown of IFI16 led to a severe attenuation of IFN-α and the IFN-stimulated gene retinoic acid-inducible gene I (RIG-I) in response to cyclic GMP-AMP, a second messenger produced by cyclic GMP-AMP synthase (cGAS) as well as RNA ligands and viruses. Analysis of IFI16 knockdown cells revealed compromised occupancy of RNA polymerase II on the IFN-α promoter in these cells, suggesting that transcription of IFN-stimulated genes is dependent on IFI16. These results indicate a broader role for IFI16 in the regulation of the type I IFN response to RNA and DNA viruses in antiviral immunity.
MeSH term(s)	Base Sequence ; DNA Primers ; DNA Viruses/immunology ; Enzyme-Linked Immunosorbent Assay ; Gene Knockdown Techniques ; Gene Silencing ; HEK293 Cells ; Humans ; Interferon Type I/biosynthesis ; Interferon Type I/genetics ; Interferon Type I/physiology ; Nuclear Proteins/genetics ; Nuclear Proteins/physiology ; Phosphoproteins/genetics ; Phosphoproteins/physiology ; Polymerase Chain Reaction ; RNA Viruses/immunology ; Transcription, Genetic
Chemical Substances	DNA Primers ; Interferon Type I ; Nuclear Proteins ; Phosphoproteins ; IFI16 protein, human (148998-64-5)
Language	English
Publishing date	2014-07-07
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2997-x
ISSN	1083-351X ; 0021-9258
ISSN (online)	1083-351X
ISSN	0021-9258
DOI	10.1074/jbc.M114.554147
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Article ; Online: Pattern recognition receptors and the innate immune response to viral infection.

Thompson, Mikayla R / Kaminski, John J / Kurt-Jones, Evelyn A / Fitzgerald, Katherine A

Viruses

2011 Volume 3, Issue 6, Page(s) 920–940

Abstract	The innate immune response to viral pathogens is critical in order to mobilize protective immunity. Cells of the innate immune system detect viral infection largely through germline-encoded pattern recognition receptors (PRRs) present either on the cell surface or within distinct intracellular compartments. These include the Toll-like receptors (TLRs), the retinoic acid-inducble gene I-like receptors (RLRs), the nucleotide oligomerization domain-like receptors (NLRs, also called NACHT, LRR and PYD domain proteins) and cytosolic DNA sensors. While in certain cases viral proteins are the trigger of these receptors, the predominant viral activators are nucleic acids. The presence of viral sensing PRRs in multiple cellular compartments allows innate cells to recognize and quickly respond to a broad range of viruses, which replicate in different cellular compartments. Here, we review the role of PRRs and associated signaling pathways in detecting viral pathogens in order to evoke production of interferons and cytokines. By highlighting recent progress in these areas, we hope to convey a greater understanding of how viruses activate PRR signaling and how this interaction shapes the anti-viral immune response.
MeSH term(s)	Animals ; Humans ; Immunity, Innate ; Receptors, Pattern Recognition/genetics ; Receptors, Pattern Recognition/immunology ; Signal Transduction ; Virus Diseases/genetics ; Virus Diseases/immunology ; Virus Diseases/virology ; Virus Physiological Phenomena ; Viruses/immunology
Chemical Substances	Receptors, Pattern Recognition
Language	English
Publishing date	2011-06-23
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2516098-9
ISSN	1999-4915 ; 1999-4915
ISSN (online)	1999-4915
ISSN	1999-4915
DOI	10.3390/v3060920
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Article ; Online: Differential expression of APE1 and APE2 in germinal centers promotes error-prone repair and A:T mutations during somatic hypermutation.

Stavnezer, Janet / Linehan, Erin K / Thompson, Mikayla R / Habboub, Ghaith / Ucher, Anna J / Kadungure, Tatenda / Tsuchimoto, Daisuke / Nakabeppu, Yusaku / Schrader, Carol E

Proceedings of the National Academy of Sciences of the United States of America

2014 Volume 111, Issue 25, Page(s) 9217–9222

Abstract: Somatic hypermutation (SHM) of antibody variable region genes is initiated in germinal center B cells during an immune response by activation-induced cytidine deaminase (AID), which converts cytosines to uracils. During accurate repair in nonmutating ... ...

Abstract	Somatic hypermutation (SHM) of antibody variable region genes is initiated in germinal center B cells during an immune response by activation-induced cytidine deaminase (AID), which converts cytosines to uracils. During accurate repair in nonmutating cells, uracil is excised by uracil DNA glycosylase (UNG), leaving abasic sites that are incised by AP endonuclease (APE) to create single-strand breaks, and the correct nucleotide is reinserted by DNA polymerase β. During SHM, for unknown reasons, repair is error prone. There are two APE homologs in mammals and, surprisingly, APE1, in contrast to its high expression in both resting and in vitro-activated splenic B cells, is expressed at very low levels in mouse germinal center B cells where SHM occurs, and APE1 haploinsufficiency has very little effect on SHM. In contrast, the less efficient homolog, APE2, is highly expressed and contributes not only to the frequency of mutations, but also to the generation of mutations at A:T base pair (bp), insertions, and deletions. In the absence of both UNG and APE2, mutations at A:T bp are dramatically reduced. Single-strand breaks generated by APE2 could provide entry points for exonuclease recruited by the mismatch repair proteins Msh2-Msh6, and the known association of APE2 with proliferating cell nuclear antigen could recruit translesion polymerases to create mutations at AID-induced lesions and also at A:T bp. Our data provide new insight into error-prone repair of AID-induced lesions, which we propose is facilitated by down-regulation of APE1 and up-regulation of APE2 expression in germinal center B cells.
MeSH term(s)	Animals ; B-Lymphocytes/cytology ; B-Lymphocytes/metabolism ; DNA Glycosylases/genetics ; DNA Glycosylases/metabolism ; DNA Repair ; DNA-(Apurinic or Apyrimidinic Site) Lyase/biosynthesis ; DNA-(Apurinic or Apyrimidinic Site) Lyase/genetics ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Endonucleases/biosynthesis ; Endonucleases/genetics ; Gene Expression Regulation, Enzymologic/physiology ; Germinal Center/cytology ; Germinal Center/metabolism ; Mice ; Mice, Knockout ; Multifunctional Enzymes ; MutS Homolog 2 Protein/genetics ; MutS Homolog 2 Protein/metabolism ; Mutation ; Proliferating Cell Nuclear Antigen/genetics ; Proliferating Cell Nuclear Antigen/metabolism ; Somatic Hypermutation, Immunoglobulin/physiology
Chemical Substances	DNA-Binding Proteins ; Msh6 protein, mouse ; Multifunctional Enzymes ; Proliferating Cell Nuclear Antigen ; Apex2 protein, mouse (EC 3.1.-) ; Endonucleases (EC 3.1.-) ; DNA Glycosylases (EC 3.2.2.-) ; Msh2 protein, mouse (EC 3.6.1.3) ; MutS Homolog 2 Protein (EC 3.6.1.3) ; Apex1 protein, mouse (EC 4.2.99.18) ; DNA-(Apurinic or Apyrimidinic Site) Lyase (EC 4.2.99.18)
Language	English
Publishing date	2014-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	209104-5
ISSN	1091-6490 ; 0027-8424
ISSN (online)	1091-6490
ISSN	0027-8424
DOI	10.1073/pnas.1405590111
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Article ; Online: CD200R1 supports HSV-1 viral replication and licenses pro-inflammatory signaling functions of TLR2.

Soberman, Roy J / MacKay, Christopher R / Vaine, Christine A / Ryan, Glennice Bowen / Cerny, Anna M / Thompson, Mikayla R / Nikolic, Boris / Primo, Valeria / Christmas, Peter / Sheiffele, Paul / Aronov, Lisa / Knipe, David M / Kurt-Jones, Evelyn A

PloS one

2012 Volume 7, Issue 10, Page(s) e47740

Abstract: The CD200R1:CD200 axis is traditionally considered to limit tissue inflammation by down-regulating pro-inflammatory signaling in myeloid cells bearing the receptor. We generated CD200R1(-/-) mice and employed them to explore both the role of CD200R1 in ... ...

Abstract	The CD200R1:CD200 axis is traditionally considered to limit tissue inflammation by down-regulating pro-inflammatory signaling in myeloid cells bearing the receptor. We generated CD200R1(-/-) mice and employed them to explore both the role of CD200R1 in regulating macrophage signaling via TLR2 as well as the host response to an in vivo, TLR2-dependent model, herpes simplex virus 1 (HSV-1) infection. CD200R1(-/-) peritoneal macrophages demonstrated a 70-75% decrease in the generation of IL-6 and CCL5 (Rantes) in response to the TLR2 agonist Pam(2)CSK(4) and to HSV-1. CD200R1(-/-) macrophages could neither up-regulate the expression of TLR2, nor assemble a functional inflammasome in response to HSV-1. CD200R1(-/-) mice were protected from HSV-1 infection and exhibited dysfunctional TLR2 signaling. Finally, both CD200R1(-/-) mice and CD200R1(-/-) fibroblasts and macrophages showed a markedly reduced ability to support HSV-1 replication. In summary, our data demonstrate an unanticipated and novel requirement for CD200R1 in "licensing" pro-inflammatory functions of TLR2 and in limiting viral replication that are supported by ex vivo and in vivo evidence.
MeSH term(s)	Animals ; Antigens, Surface/metabolism ; Brain/immunology ; Brain/pathology ; Brain/virology ; Embryo, Mammalian/cytology ; Encephalitis/immunology ; Encephalitis/pathology ; Encephalitis/virology ; Fibroblasts/metabolism ; Fibroblasts/pathology ; Fibroblasts/virology ; Gene Targeting ; Herpesvirus 1, Human/physiology ; Inflammation/immunology ; Inflammation/pathology ; Interferon Type I/biosynthesis ; Macrophages, Peritoneal/immunology ; Macrophages, Peritoneal/pathology ; Macrophages, Peritoneal/virology ; Mice ; Orexin Receptors ; Receptors, Cell Surface/deficiency ; Receptors, Cell Surface/metabolism ; Signal Transduction/immunology ; Toll-Like Receptor 2/metabolism ; Viral Load/immunology ; Virus Replication/physiology
Chemical Substances	Antigens, Surface ; Cd200r1 protein, mouse ; Interferon Type I ; Orexin Receptors ; Receptors, Cell Surface ; Tlr2 protein, mouse ; Toll-Like Receptor 2
Keywords	covid19
Language	English
Publishing date	2012-10-17
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0047740
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Article ; Online: CD200R1 supports HSV-1 viral replication and licenses pro-inflammatory signaling functions of TLR2.

Roy J Soberman / Christopher R MacKay / Christine A Vaine / Glennice Bowen Ryan / Anna M Cerny / Mikayla R Thompson / Boris Nikolic / Valeria Primo / Peter Christmas / Paul Sheiffele / Lisa Aronov / David M Knipe / Evelyn A Kurt-Jones

PLoS ONE, Vol 7, Iss 10, p e

2012 Volume 47740

Abstract	The CD200R1:CD200 axis is traditionally considered to limit tissue inflammation by down-regulating pro-inflammatory signaling in myeloid cells bearing the receptor. We generated CD200R1(-/-) mice and employed them to explore both the role of CD200R1 in regulating macrophage signaling via TLR2 as well as the host response to an in vivo, TLR2-dependent model, herpes simplex virus 1 (HSV-1) infection. CD200R1(-/-) peritoneal macrophages demonstrated a 70-75% decrease in the generation of IL-6 and CCL5 (Rantes) in response to the TLR2 agonist Pam(2)CSK(4) and to HSV-1. CD200R1(-/-) macrophages could neither up-regulate the expression of TLR2, nor assemble a functional inflammasome in response to HSV-1. CD200R1(-/-) mice were protected from HSV-1 infection and exhibited dysfunctional TLR2 signaling. Finally, both CD200R1(-/-) mice and CD200R1(-/-) fibroblasts and macrophages showed a markedly reduced ability to support HSV-1 replication. In summary, our data demonstrate an unanticipated and novel requirement for CD200R1 in "licensing" pro-inflammatory functions of TLR2 and in limiting viral replication that are supported by ex vivo and in vivo evidence.
Keywords	Medicine ; R ; Science ; Q
Subject code	570
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: Proteasomal degradation of herpes simplex virus capsids in macrophages releases DNA to the cytosol for recognition by DNA sensors.

Horan, Kristy A / Hansen, Kathrine / Jakobsen, Martin R / Holm, Christian K / Søby, Stine / Unterholzner, Leonie / Thompson, Mikayla / West, John A / Iversen, Marie B / Rasmussen, Simon B / Ellermann-Eriksen, Svend / Kurt-Jones, Evelyn / Landolfo, Santo / Damania, Blossom / Melchjorsen, Jesper / Bowie, Andrew G / Fitzgerald, Katherine A / Paludan, Søren R

Journal of immunology (Baltimore, Md. : 1950)

2013 Volume 190, Issue 5, Page(s) 2311–2319

Abstract: The innate immune system is important for control of infections, including herpesvirus infections. Intracellular DNA potently stimulates antiviral IFN responses. It is known that plasmacytoid dendritic cells sense herpesvirus DNA in endosomes via TLR9 ... ...

Abstract	The innate immune system is important for control of infections, including herpesvirus infections. Intracellular DNA potently stimulates antiviral IFN responses. It is known that plasmacytoid dendritic cells sense herpesvirus DNA in endosomes via TLR9 and that nonimmune tissue cells can sense herpesvirus DNA in the nucleus. However, it remains unknown how and where myeloid cells, such as macrophages and conventional dendritic cells, detect infections with herpesviruses. In this study, we demonstrate that the HSV-1 capsid was ubiquitinated in the cytosol and degraded by the proteasome, hence releasing genomic DNA into the cytoplasm for detection by DNA sensors. In this context, the DNA sensor IFN-γ-inducible 16 is important for induction of IFN-β in human macrophages postinfection with HSV-1 and CMV. Viral DNA localized to the same cytoplasmic regions as did IFN-γ-inducible 16, with DNA sensing being independent of viral nuclear entry. Thus, proteasomal degradation of herpesvirus capsids releases DNA to the cytoplasm for recognition by DNA sensors.
MeSH term(s)	Animals ; Capsid/metabolism ; Cell Line ; Cell Nucleus/metabolism ; Chlorocebus aethiops ; Cytomegalovirus/genetics ; Cytomegalovirus/metabolism ; Cytosol/metabolism ; DNA, Viral/genetics ; DNA, Viral/immunology ; Dendritic Cells/metabolism ; Dendritic Cells/virology ; Gene Silencing ; Herpesvirus 1, Human/genetics ; Herpesvirus 1, Human/metabolism ; Humans ; Interferon-beta/biosynthesis ; Interferon-beta/immunology ; Macrophages/metabolism ; Macrophages/virology ; Nuclear Proteins/antagonists & inhibitors ; Nuclear Proteins/immunology ; Nuclear Proteins/metabolism ; Phosphoproteins/antagonists & inhibitors ; Phosphoproteins/immunology ; Phosphoproteins/metabolism ; Proteasome Endopeptidase Complex/metabolism ; RNA, Small Interfering/genetics ; Ubiquitination ; Vero Cells
Chemical Substances	DNA, Viral ; Nuclear Proteins ; Phosphoproteins ; RNA, Small Interfering ; IFI16 protein, human (148998-64-5) ; Interferon-beta (77238-31-4) ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2013-01-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1202749
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In stock of ZB MED Cologne/Königswinter

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