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Article ; Online: Genetic Versus Non-genetic Drivers of SLE: Implications of IRF5 Dysregulation in Both Roads Leading to SLE.

Barnes, Betsy J

2019 Volume 21, Issue 1, Page(s) 2

Abstract: Purpose of review: Systemic lupus erythematosus (SLE) is characterized by a breakdown of immune tolerance, resulting in inflammation and tissue destruction. While the primary causes of SLE are still obscure, the disorder is highly heritable. Genetic ... ...

Abstract	Purpose of review: Systemic lupus erythematosus (SLE) is characterized by a breakdown of immune tolerance, resulting in inflammation and tissue destruction. While the primary causes of SLE are still obscure, the disorder is highly heritable. Genetic risk variants, on their own, are rarely causal or fully explain disease pathogenesis. We discuss the possibility that IRF5, a SLE susceptibility gene, has both genetic and non-genetic contributions to disease pathogenesis. Recent findings: Genetic variants within and around IRF5 robustly associate with SLE risk. In SLE blood cells, IRF5 risk variants associate with elevated IRF5 expression and IFN production. Whether the observed increase in expression is due to risk variants or other disease-associated factors is not clear. Data from Irf5
MeSH term(s)	Animals ; Gene Expression Regulation/immunology ; Genetic Predisposition to Disease ; Humans ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/immunology ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Polymorphism, Single Nucleotide
Chemical Substances	IRF5 protein, human ; Interferon Regulatory Factors
Language	English
Publishing date	2019-01-15
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2057357-1
ISSN	1534-6307 ; 1523-3774
ISSN (online)	1534-6307
ISSN	1523-3774
DOI	10.1007/s11926-019-0803-3
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Zs.A 5531: Show issues

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Article ; Online: Role of interferon regulatory factor 5 (IRF5) in tumor progression: Prognostic and therapeutic potential.

Roberts, Bailey K / Collado, Gilbert / Barnes, Betsy J

Biochimica et biophysica acta. Reviews on cancer

2023 Volume 1879, Issue 1, Page(s) 189061

Abstract: Canonically, the transcription factor interferon regulatory factor 5 (IRF5) is a key mediator of innate and adaptive immunity downstream of pathogen recognition receptors such as Toll-like receptors (TLRs). Hence, dysregulation of IRF5 function has been ... ...

Abstract	Canonically, the transcription factor interferon regulatory factor 5 (IRF5) is a key mediator of innate and adaptive immunity downstream of pathogen recognition receptors such as Toll-like receptors (TLRs). Hence, dysregulation of IRF5 function has been widely implicated in inflammatory and autoimmune diseases. Over the last few decades, dysregulation of IRF5 expression has been also reported in hematologic malignancies and solid cancers that support a role for IRF5 in malignant transformation, tumor immune regulation, clinical prognosis, and treatment response. This review will provide an in-depth overview of the current literature regarding the mechanisms by which IRF5 functions as either a tumor suppressor or oncogene, its role in metastasis, regulation of the tumor-immune microenvironment, utility as a prognostic indicator of disease, and new developments in IRF5 therapeutics that may be used to remodel tumor immunity.
MeSH term(s)	Humans ; Prognosis ; Interferon Regulatory Factors/genetics ; Interferon Regulatory Factors/metabolism ; Gene Expression Regulation ; Adaptive Immunity
Chemical Substances	Interferon Regulatory Factors ; IRF5 protein, human
Language	English
Publishing date	2023-12-21
Publishing country	Netherlands
Document type	Journal Article ; Review
ZDB-ID	2918802-7
ISSN	1879-2561 ; 0304-419X
ISSN (online)	1879-2561
ISSN	0304-419X
DOI	10.1016/j.bbcan.2023.189061
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Article ; Online: A New Methodology for the Quantification of Neutrophil Extracellular Traps in Patient Plasma.

Matta, Bharati / Battaglia, Jenna / Barnes, Betsy J

Bio-protocol

2023 Volume 13, Issue 12, Page(s) e4701

Abstract: Neutrophil extracellular traps (NETs) are web-like structures made up of decondensed chromatin fibers along with neutrophil granular proteins that are extruded by neutrophils after activation or in response to foreign microorganisms. NETs have been ... ...

Abstract	Neutrophil extracellular traps (NETs) are web-like structures made up of decondensed chromatin fibers along with neutrophil granular proteins that are extruded by neutrophils after activation or in response to foreign microorganisms. NETs have been associated with autoimmune and inflammatory diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis, coronavirus disease 2019 (COVID-19), and others. There are reliable methods available to quantitate NETs from neutrophils, but their accurate quantification in patient plasma or serum remains a challenge. We developed a highly sensitive ELISA to detect NETs in serum/plasma and designed a novel smear immunofluorescence assay to detect NETs in as little as 1 μL of serum/plasma. We further validated our technology on plasma samples from SLE patients and healthy donors that carry interferon regulatory factor 5 genetic risk. The multiplex ELISA combines the use of three antibodies against myeloperoxidase (MPO), citrullinated histone H3 (CitH3), and DNA to detect the NET complexes with higher specificities. The immunofluorescence smear assay can visually detect intact structures of NETs in 1 μL of serum/plasma and provide similar results that correlate with findings from the multiplex ELISA. Furthermore, the smear assay is a relatively simple, inexpensive, and quantifiable method of NET detection for small volumes.
Language	English
Publishing date	2023-06-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4701
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Article ; Online: Intracellular IRF5 Dimerization Assay.

Sherman, Cherrie D / Barnes, Betsy J

Bio-protocol

2021 Volume 11, Issue 10, Page(s) e4021

Abstract: The intracellular interferon regulatory factor 5 (IRF5) dimerization assay is a technique designed to measure molecular interaction(s) with endogenous IRF5. Here, we present two methods that detect endogenous IRF5 homodimerization and interaction of ... ...

Abstract	The intracellular interferon regulatory factor 5 (IRF5) dimerization assay is a technique designed to measure molecular interaction(s) with endogenous IRF5. Here, we present two methods that detect endogenous IRF5 homodimerization and interaction of endogenous IR5 with cell penetrating peptide (CPP) inhibitors. Briefly, to detect endogenous IRF5 dimers, THP-1 cells are incubated in the presence or absence of the IRF5-targeted CPP (IRF5-CPP) inhibitor for 30 min then the cells are stimulated with R848 for 1 h. Cell lysates are separated by native-polyacrylamide gel electrophoresis (PAGE) and IRF5 dimers are detected by immunoblotting with IRF5 antibodies. To detect endogenous interactions between IRF5 and FITC-labeled IRF5-CPP, an in-cell fluorescence resonance energy transfer (FRET) assay is used. In this assay, THP-1 cells are left untreated or treated with FITC-IRF5-CPP conjugated inhibitors for 1 h. Next, cells are fixed, permeabilized, and stained with anti-IRF5 and TRITC-conjugated secondary antibodies. Transfer of fluorescence can be measured and calculated as FRET units. These methods provide rapid and accurate assays to detect IRF5 molecular interactions.
Language	English
Publishing date	2021-05-20
Publishing country	United States
Document type	Journal Article
ZDB-ID	2833269-6
ISSN	2331-8325 ; 2331-8325
ISSN (online)	2331-8325
ISSN	2331-8325
DOI	10.21769/BioProtoc.4021
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Article ; Online: Navigating the marrow sea towards erythromyeloblastic islands under normal and inflammatory conditions.

Josselsohn, Rachel / Barnes, Betsy J / Kalfa, Theodosia A / Blanc, Lionel

Current opinion in hematology

2023 Volume 30, Issue 3, Page(s) 80–85

Abstract: Purpose of review: Terminal erythroid differentiation occurs in specialized niches called erythroblastic islands. Since their discovery in 1958, these niches have been described as a central macrophage surrounded by differentiating erythroblasts. Here, ... ...

Abstract	Purpose of review: Terminal erythroid differentiation occurs in specialized niches called erythroblastic islands. Since their discovery in 1958, these niches have been described as a central macrophage surrounded by differentiating erythroblasts. Here, we review the recent advances made in the characterization of these islands and the role they could play in anaemia of inflammation. Recent findings: The utilization of multispectral imaging flow cytometry (flow cytometry with microscopy) has enabled for a more precise characterization of the niche that revealed the presence of maturing granulocytes in close contact with the central macrophage. These erythromyeloblastic islands (EMBIs) can adapt depending on the peripheral needs. Indeed, during inflammation wherein inflammatory cytokines limit erythropoiesis and promote granulopoiesis, EMBIs present altered structures with increased maturing granulocytes and decreased erythroid precursors. Summary: Regulation of the structure and function of the EMBI in the bone marrow emerges as a potential player in the pathophysiology of acute and chronic inflammation and its associated anaemia.
MeSH term(s)	Humans ; Bone Marrow/physiology ; Erythroblasts ; Erythropoiesis/physiology ; Anemia/etiology ; Inflammation
Language	English
Publishing date	2023-01-17
Publishing country	United States
Document type	Review ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1153887-9
ISSN	1531-7048 ; 1065-6251
ISSN (online)	1531-7048
ISSN	1065-6251
DOI	10.1097/MOH.0000000000000756
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Article ; Online: Detection of neutrophil extracellular traps in patient plasma: method development and validation in systemic lupus erythematosus and healthy donors that carry

Matta, Bharati / Battaglia, Jenna / Barnes, Betsy J

Frontiers in immunology

2022 Volume 13, Page(s) 951254

Abstract: Neutrophil extracellular traps (NETs) are web-like structures extruded by neutrophils after activation or in response to microorganisms. These extracellular structures are decondensed chromatin fibers loaded with antimicrobial granular proteins, peptides, ...

Abstract	Neutrophil extracellular traps (NETs) are web-like structures extruded by neutrophils after activation or in response to microorganisms. These extracellular structures are decondensed chromatin fibers loaded with antimicrobial granular proteins, peptides, and enzymes. NETs clear microorganisms, thus keeping a check on infections at an early stage, but if dysregulated, may be self-destructive to the body. Indeed, NETs have been associated with autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), antiphospholipid syndrome (APS), psoriasis, and gout. More recently, increased NETs associate with COVID-19 disease severity. While there are rigorous and reliable methods to quantify NETs from neutrophils
MeSH term(s)	COVID-19 ; Extracellular Traps ; Humans ; Interferon Regulatory Factors/metabolism ; Lupus Erythematosus, Systemic ; Neutrophils
Chemical Substances	IRF5 protein, human ; Interferon Regulatory Factors
Language	English
Publishing date	2022-07-26
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2022.951254
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Article ; Online: Modulating Cytokine Production via Select Packaging and Secretion From Extracellular Vesicles.

Barnes, Betsy J / Somerville, Carter C

Frontiers in immunology

2020 Volume 11, Page(s) 1040

Abstract: Cytokines are soluble factors that play vital roles in systemic function due to their ability to initiate and mediate cell-to-cell communication. Another important mechanism of intercellular communication that has gained significant attention in the past ...

Abstract	Cytokines are soluble factors that play vital roles in systemic function due to their ability to initiate and mediate cell-to-cell communication. Another important mechanism of intercellular communication that has gained significant attention in the past 10 years is the release of extracellular vesicles (EVs). EVs are released by all cells during normal physiology, in states of resting and activation, as well as during disease. Accumulating evidence indicates that cytokines may be packaged into EVs, and the packaging of cytokines into EVs, along with their ultimate secretion, may also be regulated by cytokines. Importantly, the repertoire of biomolecules packaged into EVs is shaped by the biological state of the cell (resting vs. activated and healthy vs. disease) and the EV biogenesis pathway involved, thus providing mechanisms by which EV packaging and secretion may be modulated. Given the critical role of cytokines in driving acute and chronic inflammatory and autoimmune diseases, as well as their role in establishing the tumor immune microenvironment, in this review, we will focus on these disease settings and summarize recent progress and mechanisms by which cytokines may be packaged within and modulated by EVs, as a therapeutic option for regulating innate and adaptive immunity.
MeSH term(s)	Adaptive Immunity ; Animals ; Autoimmune Diseases/immunology ; Cytokines/metabolism ; Extracellular Vesicles/metabolism ; Humans ; Immunity, Innate ; Immunomodulation ; Immunotherapy ; Inflammation/immunology ; Neoplasms/immunology ; Tumor Microenvironment
Chemical Substances	Cytokines
Language	English
Publishing date	2020-05-29
Publishing country	Switzerland
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01040
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Article ; Online: Coordination between innate immune cells, type I IFNs and IRF5 drives SLE pathogenesis.

Matta, Bharati / Barnes, Betsy J

Cytokine

2019 Volume 132, Page(s) 154731

Abstract: Systemic lupus erythematosus (SLE) is a complex autoimmune disease which affects multiple organs. The type I interferon (IFN) gene signature and circulating autoantibodies are hallmarks of SLE. Plasmacytoid dendritic cells (pDCs) are considered the main ... ...

Abstract	Systemic lupus erythematosus (SLE) is a complex autoimmune disease which affects multiple organs. The type I interferon (IFN) gene signature and circulating autoantibodies are hallmarks of SLE. Plasmacytoid dendritic cells (pDCs) are considered the main producers of type I IFN and production is modulated by multiple other immune cell types. In SLE, essentially every immune cell type is dysregulated and aberrant deregulation is thought to be due, in part, to direct or indirect exposure to IFN. Genetic variants within or around the transcription factor interferon regulatory factor 5 (IRF5) associate with SLE risk. Elevated IFNα activity was detected in the sera of SLE patients carrying IRF5 risk polymorphisms who were positive for either anti-RNA binding protein (anti-RBP) or anti-double-stranded DNA (anti-dsDNA) autoantibodies. Neutrophils are also an important source of type I IFNs and are found in abundance in human blood. Neutrophil extracellular traps (NETs) are considered a potential source of antigenic trigger in SLE that can lead to type I IFN gene induction, as well as increased autoantibody production. In this review, we will focus on immune cell types that produce type I IFNs and/or are affected by type I IFN in SLE. In addition, we will discuss potential inducers of endogenous type I IFN production in SLE. Last, we will postulate how the different immune cell populations may be affected by an IRF5-SLE risk haplotype.
Language	English
Publishing date	2019-05-23
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S. ; Research Support, Non-U.S. Gov't
ZDB-ID	1018055-2
ISSN	1096-0023 ; 1043-4666
ISSN (online)	1096-0023
ISSN	1043-4666
DOI	10.1016/j.cyto.2019.05.018
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Zs.A 2840: Show issues

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Article ; Online: Retraction for Korczeniewska and Barnes, "The COP9 Signalosome Interacts with and Regulates Interferon Regulatory Factor 5 Protein Stability".

Korczeniewska, Justyna / Barnes, Betsy J

Molecular and cellular biology

2017 Volume 37, Issue 24

Language	English
Publishing date	2017--15
Publishing country	United States
Document type	Journal Article ; Retraction of Publication
ZDB-ID	779397-2
ISSN	1098-5549 ; 0270-7306
ISSN (online)	1098-5549
ISSN	0270-7306
DOI	10.1128/MCB.00477-17
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Article ; Online: Potential T Cell-Intrinsic Regulatory Roles for IRF5 via Cytokine Modulation in T Helper Subset Differentiation and Function.

Brune, Zarina / Rice, Matthew R / Barnes, Betsy J

Frontiers in immunology

2020 Volume 11, Page(s) 1143

Abstract: Interferon Regulatory Factor 5 (IRF5) is one of nine members of the IRF family of transcription factors. Although initially discovered as a key regulator of the type I interferon and pro-inflammatory cytokine arm of the innate immune response, IRF5 has ... ...

Abstract	Interferon Regulatory Factor 5 (IRF5) is one of nine members of the IRF family of transcription factors. Although initially discovered as a key regulator of the type I interferon and pro-inflammatory cytokine arm of the innate immune response, IRF5 has now been found to also mediate pathways involved in cell growth and differentiation, apoptosis, metabolic homeostasis and tumor suppression. Hyperactivation of IRF5 has been implicated in numerous autoimmune diseases, chief among them systemic lupus erythematosus (SLE). SLE is a heterogeneous autoimmune disease in which patients often share similar characteristics in terms of autoantibody production and strong genetic risk factors, yet also possess unique disease signatures.
MeSH term(s)	Animals ; Cell Differentiation/immunology ; Cytokines/immunology ; Humans ; Interferon Regulatory Factors/immunology ; Lupus Erythematosus, Systemic/immunology ; Mice ; T-Lymphocyte Subsets/immunology ; T-Lymphocytes, Helper-Inducer/immunology
Chemical Substances	Cytokines ; Interferon Regulatory Factors
Language	English
Publishing date	2020-06-03
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.01143
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