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Article: Type I Interferon Is a Catastrophic Feature of the Diabetic Islet Microenvironment.

Newby, Brittney N / Mathews, Clayton E

2017 Volume 8, Page(s) 232

Abstract: A detailed understanding of the molecular pathways and cellular interactions that result in islet beta cell (β cell) destruction is essential for the development and implementation of effective therapies for prevention or reversal of type 1 diabetes (T1D) ...

Abstract	A detailed understanding of the molecular pathways and cellular interactions that result in islet beta cell (β cell) destruction is essential for the development and implementation of effective therapies for prevention or reversal of type 1 diabetes (T1D). However, events that define the pathogenesis of human T1D have remained elusive. This gap in our knowledge results from the complex interaction between genetics, the immune system, and environmental factors that precipitate T1D in humans. A link between genetics, the immune system, and environmental factors are type 1 interferons (T1-IFNs). These cytokines are well known for inducing antiviral factors that limit infection by regulating innate and adaptive immune responses. Further, several T1D genetic risk loci are within genes that link innate and adaptive immune cell responses to T1-IFN. An additional clue that links T1-IFN to T1D is that these cytokines are a known constituent of the autoinflammatory milieu within the pancreas of patients with T1D. The presence of IFNα/β is correlated with characteristic MHC class I (MHC-I) hyperexpression found in the islets of patients with T1D, suggesting that T1-IFNs modulate the cross-talk between autoreactive cytotoxic CD8
Language	English
Publishing date	2017-09-14
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2017.00232
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Article ; Online: In search of a surrogate: engineering human beta cell lines for therapy.

Newby, Brittney N / Terada, Naohiro / Mathews, Clayton E

Trends in endocrinology and metabolism: TEM

2014 Volume 25, Issue 8, Page(s) 378–380

Abstract: Replacement of insulin-producing cells is a promising therapy for the restoration of the beta cell mass that is destroyed in patients with type 1 diabetes (T1D). However, the use of large amounts of islets per transplant, coupled with the scarcity of ... ...

Abstract	Replacement of insulin-producing cells is a promising therapy for the restoration of the beta cell mass that is destroyed in patients with type 1 diabetes (T1D). However, the use of large amounts of islets per transplant, coupled with the scarcity of donor tissue, diminishes its feasibility. Here we briefly discuss current progress in developing ideal functional beta cells as well as the rationale for developing renewable sources of insulin-producing cells that can be transplanted.
MeSH term(s)	Cell Line ; Diabetes Mellitus, Type 1/therapy ; Humans ; Insulin-Secreting Cells/cytology ; Insulin-Secreting Cells/transplantation ; Islets of Langerhans Transplantation/methods
Language	English
Publishing date	2014-06-20
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1042384-9
ISSN	1879-3061 ; 1043-2760
ISSN (online)	1879-3061
ISSN	1043-2760
DOI	10.1016/j.tem.2014.05.006
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Zs.A 2999: Show issues

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Article ; Online: Immune Mechanisms and Pathways Targeted in Type 1 Diabetes.

Jacobsen, Laura M / Newby, Brittney N / Perry, Daniel J / Posgai, Amanda L / Haller, Michael J / Brusko, Todd M

Current diabetes reports

2018 Volume 18, Issue 10, Page(s) 90

Abstract: Purpose of review: The immunosuppressive agent cyclosporine was first reported to lower daily insulin dose and improve glycemic control in patients with new-onset type 1 diabetes (T1D) in 1984. While renal toxicity limited cyclosporine's extended use, ... ...

Abstract	Purpose of review: The immunosuppressive agent cyclosporine was first reported to lower daily insulin dose and improve glycemic control in patients with new-onset type 1 diabetes (T1D) in 1984. While renal toxicity limited cyclosporine's extended use, this observation ignited collaborative efforts to identify immunotherapeutic agents capable of safely preserving β cells in patients with or at risk for T1D. Recent findings: Advances in T1D prediction and early diagnosis, together with expanded knowledge of the disease mechanisms, have facilitated trials targeting specific immune cell subsets, autoantigens, and pathways. In addition, clinical responder and non-responder subsets have been defined through the use of metabolic and immunological readouts. Herein, we review emerging T1D biomarkers within the context of recent and ongoing T1D immunotherapy trials. We also discuss responder/non-responder analyses in an effort to identify therapeutic mechanisms, define actionable pathways, and guide subject selection, drug dosing, and tailored combination drug therapy for future T1D trials.
MeSH term(s)	Autoimmunity ; Biomarkers/blood ; Diabetes Mellitus, Type 1/blood ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/therapy ; Humans ; Immunotherapy ; Primary Prevention ; T-Lymphocytes/immunology
Chemical Substances	Biomarkers
Language	English
Publishing date	2018-08-30
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	2065167-3
ISSN	1539-0829 ; 1534-4827
ISSN (online)	1539-0829
ISSN	1534-4827
DOI	10.1007/s11892-018-1066-5
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Zs.A 5628: Show issues

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Article: Use of Induced Pluripotent Stem Cells to Build Isogenic Systems and Investigate Type 1 Diabetes.

Frontiers in endocrinology

2021 Volume 12, Page(s) 737276

Abstract: Type 1 diabetes (T1D) is a disease that arises due to complex immunogenetic mechanisms. Key cell-cell interactions involved in the pathogenesis of T1D are activation of autoreactive T cells by dendritic cells (DC), migration of T cells across endothelial ...

Abstract	Type 1 diabetes (T1D) is a disease that arises due to complex immunogenetic mechanisms. Key cell-cell interactions involved in the pathogenesis of T1D are activation of autoreactive T cells by dendritic cells (DC), migration of T cells across endothelial cells (EC) lining capillary walls into the islets of Langerhans, interaction of T cells with macrophages in the islets, and killing of β-cells by autoreactive CD8
MeSH term(s)	CD8-Positive T-Lymphocytes/pathology ; Cell Differentiation/physiology ; Diabetes Mellitus, Type 1/pathology ; Humans ; Induced Pluripotent Stem Cells/pathology ; Insulin-Secreting Cells/pathology ; Islets of Langerhans/pathology
Language	English
Publishing date	2021-11-09
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2592084-4
ISSN	1664-2392
ISSN	1664-2392
DOI	10.3389/fendo.2021.737276
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Article ; Online: Innate inflammation drives NK cell activation to impair Treg activity.

Dean, Joseph W / Peters, Leeana D / Fuhrman, Christopher A / Seay, Howard R / Posgai, Amanda L / Stimpson, Scott E / Brusko, Maigan A / Perry, Daniel J / Yeh, Wen-I / Newby, Brittney N / Haller, Michael J / Muir, Andrew B / Atkinson, Mark A / Mathews, Clayton E / Brusko, Todd M

Journal of autoimmunity

2020 Volume 108, Page(s) 102417

Abstract: IL-12 and IL-18 synergize to promote ... ...

Abstract	IL-12 and IL-18 synergize to promote T
MeSH term(s)	Adolescent ; Adult ; Biomarkers ; Cells, Cultured ; Child ; Cytokines/metabolism ; Cytotoxicity, Immunologic ; Diabetes Mellitus, Type 1/etiology ; Diabetes Mellitus, Type 1/metabolism ; Disease Susceptibility ; Female ; Humans ; Immunity, Innate ; Immunophenotyping ; Inflammation/immunology ; Inflammation/metabolism ; Inflammation/pathology ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Lymphocyte Activation/immunology ; Lymphocyte Count ; Male ; Middle Aged ; Models, Biological ; Phenotype ; Quantitative Trait Loci ; T-Lymphocytes, Cytotoxic/immunology ; T-Lymphocytes, Cytotoxic/metabolism ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; Young Adult
Chemical Substances	Biomarkers ; Cytokines
Language	English
Publishing date	2020-02-06
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	639452-8
ISSN	1095-9157 ; 0896-8411
ISSN (online)	1095-9157
ISSN	0896-8411
DOI	10.1016/j.jaut.2020.102417
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Zs.A 2368: Show issues

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Article ; Online: Type 1 Interferons Potentiate Human CD8

Newby, Brittney N / Brusko, Todd M / Zou, Baiming / Atkinson, Mark A / Clare-Salzler, Michael / Mathews, Clayton E

Diabetes

2017 Volume 66, Issue 12, Page(s) 3061–3071

Abstract: Events defining the progression to human type 1 diabetes (T1D) have remained elusive owing to the complex interaction between genetics, the immune system, and the environment. Type 1 interferons (T1-IFN) are known to be a constituent of the ... ...

Abstract	Events defining the progression to human type 1 diabetes (T1D) have remained elusive owing to the complex interaction between genetics, the immune system, and the environment. Type 1 interferons (T1-IFN) are known to be a constituent of the autoinflammatory milieu within the pancreas of patients with T1D. However, the capacity of IFNα/β to modulate human activated autoreactive CD8
MeSH term(s)	Adolescent ; Adult ; CD8-Positive T-Lymphocytes/immunology ; Child ; Cytotoxicity, Immunologic/drug effects ; Female ; Granzymes/genetics ; Granzymes/physiology ; Humans ; Interferon Type I/pharmacology ; Male ; Promoter Regions, Genetic ; STAT4 Transcription Factor/physiology ; Young Adult
Chemical Substances	Interferon Type I ; STAT4 Transcription Factor ; STAT4 protein, human ; GZMB protein, human (EC 3.4.21.-) ; Granzymes (EC 3.4.21.-)
Language	English
Publishing date	2017-09-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db17-0106
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Article ; Online: NADPH Oxidase 2-Derived Reactive Oxygen Species Promote CD8+ T Cell Effector Function.

Chen, Jing / Liu, Chao / Chernatynskaya, Anna V / Newby, Brittney / Brusko, Todd M / Xu, Yuan / Barra, Jessie M / Morgan, Nadine / Santarlas, Christopher / Reeves, Westley H / Tse, Hubert M / Leiding, Jennifer W / Mathews, Clayton E

Journal of immunology (Baltimore, Md. : 1950)

2023 Volume 212, Issue 2, Page(s) 258–270

Abstract: Oxidants participate in lymphocyte activation and function. We previously demonstrated that eliminating the activity of NADPH oxidase 2 (NOX2) significantly impaired the effectiveness of autoreactive CD8+ CTLs. However, the molecular mechanisms impacting ...

Abstract	Oxidants participate in lymphocyte activation and function. We previously demonstrated that eliminating the activity of NADPH oxidase 2 (NOX2) significantly impaired the effectiveness of autoreactive CD8+ CTLs. However, the molecular mechanisms impacting CD8+ T cell function remain unknown. In the present study, we examined the role of NOX2 in both NOD mouse and human CD8+ T cell function. Genetic ablation or chemical inhibition of NOX2 in CD8+ T cells significantly suppressed activation-induced expression of the transcription factor T-bet, the master transcription factor of the Tc1 cell lineage, and T-bet target effector genes such as IFN-γ and granzyme B. Inhibition of NOX2 in both human and mouse CD8+ T cells prevented target cell lysis. We identified that superoxide generated by NOX2 must be converted into hydrogen peroxide to transduce the redox signal in CD8+ T cells. Furthermore, we show that NOX2-generated oxidants deactivate the tumor suppressor complex leading to activation of RheB and subsequently mTOR complex 1. These results indicate that NOX2 plays a nonredundant role in TCR-mediated CD8+ T cell effector function.
MeSH term(s)	Animals ; Humans ; Mice ; CD8-Positive T-Lymphocytes/cytology ; CD8-Positive T-Lymphocytes/immunology ; Cytokines/immunology ; Granzymes/metabolism ; Hydrogen Peroxide/metabolism ; Inflammation/immunology ; Interferon-gamma/metabolism ; Lymphocyte Activation ; Mice, Inbred NOD ; NADPH Oxidase 2/antagonists & inhibitors ; NADPH Oxidase 2/metabolism ; Oxidation-Reduction ; Reactive Oxygen Species/metabolism ; Receptors, Antigen, T-Cell/metabolism ; Signal Transduction ; T-Box Domain Proteins/metabolism ; Male ; Female ; Young Adult
Chemical Substances	acetovanillone (B6J7B9UDTR) ; Cytokines ; Granzymes (EC 3.4.21.-) ; Hydrogen Peroxide (BBX060AN9V) ; Interferon-gamma (82115-62-6) ; NADPH Oxidase 2 (EC 1.6.3.-) ; Reactive Oxygen Species ; Receptors, Antigen, T-Cell ; T-Box Domain Proteins
Language	English
Publishing date	2023-12-11
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.2200691
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Article ; Online: A Wisp3 Cre-knockin allele produces efficient recombination in spermatocytes during early prophase of meiosis I.

Hann, Steven / Kvenvold, Laura / Newby, Brittney N / Hong, Minh / Warman, Matthew L

PloS one

2013 Volume 8, Issue 9, Page(s) e75116

Abstract: Individuals with the autosomal recessive skeletal disorder Progressive Pseudorheumatoid Dysplasia have loss-of-function mutations in WISP3, and aberrant WISP3 expression has been detected in tumors from patients with colon and breast cancer. In mice ... ...

Abstract	Individuals with the autosomal recessive skeletal disorder Progressive Pseudorheumatoid Dysplasia have loss-of-function mutations in WISP3, and aberrant WISP3 expression has been detected in tumors from patients with colon and breast cancer. In mice however, neither absence nor over-expression of WISP3 was found to cause a phenotype, and endogenous Wisp3 expression has been difficult to detect. To confirm that Wisp3 knockout mice have no phenotype and to identify potential sites of endogenous Wisp3 expression, we generated mice with a knockin allele (Wisp3 (GFP-Cre)) designed to express Green Fluorescent Protein (GFP) and Cre-recombinase instead of WISP3. Heterozygous and homozygous knockin mice were fertile and indistinguishable from their wild-type littermates, confirming that mice lacking Wisp3 have no phenotype. We could not detect GFP-expression from the knockin allele, but we could detect Cre-expression after crossing mice with the knockin allele to Cre-reporter mice; the double heterozygous offspring had evidence of Cre-mediated recombination in several tissues. The only tissue that had high levels of Cre-mediated recombination was the testis, where recombination in spermatocytes occurred by early prophase of meiosis I. As a consequence, males that were double heterozygous for a Wisp3 (GFP-Cre) and a floxed allele only contributed a recombined allele to their offspring. We detected no evidence of Cre-mediated recombination in the female ovary, although when double heterozygous females contributed the reporter allele to their offspring it had recombined ~7% of the time. Wisp3 (GFP-Cre) expression therefore occurs less frequently and most likely at a later stage of oocyte development in female mice compared to male mice. We conclude that although WISP3 is dispensable in mice, male mice with a Wisp3 (GFP-Cre) allele (Jackson Laboratory stock # 017685) will be useful for studying early prophase of meiosis I and for efficiently recombining floxed alleles that are passed to offspring.
MeSH term(s)	Alleles ; Animals ; Base Sequence ; CCN Intercellular Signaling Proteins/biosynthesis ; CCN Intercellular Signaling Proteins/genetics ; Exons/genetics ; Female ; Gene Expression Regulation ; Gene Knock-In Techniques/methods ; Green Fluorescent Proteins/genetics ; Humans ; Integrases/metabolism ; Male ; Mice ; Peptide Chain Initiation, Translational ; Prophase/genetics ; Recombination, Genetic ; Spermatocytes/cytology ; Spermatocytes/metabolism
Chemical Substances	CCN Intercellular Signaling Proteins ; CCN6 protein, mouse ; Green Fluorescent Proteins (147336-22-9) ; Cre recombinase (EC 2.7.7.-) ; Integrases (EC 2.7.7.-)
Language	English
Publishing date	2013-09-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0075116
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Article ; Online: A Wisp3 Cre-knockin allele produces efficient recombination in spermatocytes during early prophase of meiosis I.

Steven Hann / Laura Kvenvold / Brittney N Newby / Minh Hong / Matthew L Warman

PLoS ONE, Vol 8, Iss 9, p e

2013 Volume 75116

Abstract	Individuals with the autosomal recessive skeletal disorder Progressive Pseudorheumatoid Dysplasia have loss-of-function mutations in WISP3, and aberrant WISP3 expression has been detected in tumors from patients with colon and breast cancer. In mice however, neither absence nor over-expression of WISP3 was found to cause a phenotype, and endogenous Wisp3 expression has been difficult to detect. To confirm that Wisp3 knockout mice have no phenotype and to identify potential sites of endogenous Wisp3 expression, we generated mice with a knockin allele (Wisp3 (GFP-Cre)) designed to express Green Fluorescent Protein (GFP) and Cre-recombinase instead of WISP3. Heterozygous and homozygous knockin mice were fertile and indistinguishable from their wild-type littermates, confirming that mice lacking Wisp3 have no phenotype. We could not detect GFP-expression from the knockin allele, but we could detect Cre-expression after crossing mice with the knockin allele to Cre-reporter mice; the double heterozygous offspring had evidence of Cre-mediated recombination in several tissues. The only tissue that had high levels of Cre-mediated recombination was the testis, where recombination in spermatocytes occurred by early prophase of meiosis I. As a consequence, males that were double heterozygous for a Wisp3 (GFP-Cre) and a floxed allele only contributed a recombined allele to their offspring. We detected no evidence of Cre-mediated recombination in the female ovary, although when double heterozygous females contributed the reporter allele to their offspring it had recombined ~7% of the time. Wisp3 (GFP-Cre) expression therefore occurs less frequently and most likely at a later stage of oocyte development in female mice compared to male mice. We conclude that although WISP3 is dispensable in mice, male mice with a Wisp3 (GFP-Cre) allele (Jackson Laboratory stock # 017685) will be useful for studying early prophase of meiosis I and for efficiently recombining floxed alleles that are passed to offspring.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
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Article ; Online: Interferon-γ Limits Diabetogenic CD8

Driver, John P / Racine, Jeremy J / Ye, Cheng / Lamont, Deanna J / Newby, Brittney N / Leeth, Caroline M / Chapman, Harold D / Brusko, Todd M / Chen, Yi-Guang / Mathews, Clayton E / Serreze, David V

Diabetes

2016 Volume 66, Issue 3, Page(s) 710–721

Abstract: Type 1 diabetes development in the NOD mouse model is widely reported to be dependent on high-level production by autoreactive ... ...

Abstract	Type 1 diabetes development in the NOD mouse model is widely reported to be dependent on high-level production by autoreactive CD4
MeSH term(s)	Adoptive Transfer ; Animals ; CD8-Positive T-Lymphocytes/drug effects ; CD8-Positive T-Lymphocytes/immunology ; Cells, Cultured ; Diabetes Mellitus, Type 1/immunology ; Female ; Humans ; Interferon-gamma/genetics ; Interferon-gamma/immunology ; Interferon-gamma/pharmacology ; Lymphocyte Activation/drug effects ; Lymphocyte Activation/immunology ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; RNA, Messenger/metabolism ; Receptors, Antigen, T-Cell/genetics ; Reverse Transcriptase Polymerase Chain Reaction ; STAT1 Transcription Factor/metabolism ; STAT4 Transcription Factor/metabolism ; Spleen/cytology ; T-Lymphocytes, Regulatory/drug effects ; T-Lymphocytes, Regulatory/immunology
Chemical Substances	RNA, Messenger ; Receptors, Antigen, T-Cell ; STAT1 Transcription Factor ; STAT4 Transcription Factor ; Stat1 protein, mouse ; Stat4 protein, mouse ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2016-12-05
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db16-0846
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