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  1. Article ; Online: Early-life microbiota-immune homeostasis.

    Reynolds, Hayley M / Bettini, Matthew L

    Frontiers in immunology

    2023  Volume 14, Page(s) 1266876

    Abstract: As the prevalence of allergy and autoimmune disease in industrialized societies continues to rise, improving our understanding of the mechanistic roles behind microbiota-immune homeostasis has become critical for informing therapeutic interventions in ... ...

    Abstract As the prevalence of allergy and autoimmune disease in industrialized societies continues to rise, improving our understanding of the mechanistic roles behind microbiota-immune homeostasis has become critical for informing therapeutic interventions in cases of dysbiosis. Of particular importance, are alterations to intestinal microbiota occurring within the critical neonatal window, during which the immune system is highly vulnerable to environmental exposures. This review will highlight recent literature concerning mechanisms of early-life microbiota-immune homeostasis as well as discuss the potential for therapeutics in restoring dysbiosis in early life.
    MeSH term(s) Infant, Newborn ; Humans ; Probiotics/therapeutic use ; Dysbiosis ; Microbiota ; Gastrointestinal Microbiome ; Homeostasis
    Language English
    Publishing date 2023-10-23
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2023.1266876
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  2. Article ; Online: Function, Failure, and the Future Potential of Tregs in Type 1 Diabetes.

    Bettini, Maria / Bettini, Matthew L

    Diabetes

    2021  Volume 70, Issue 6, Page(s) 1211–1219

    Abstract: Critical insights into the etiology of type 1 diabetes (T1D) came from genome-wide association studies that unequivocally connected genetic susceptibility to immune cell function. At the top of the susceptibility are genes involved in regulatory T-cell ( ... ...

    Abstract Critical insights into the etiology of type 1 diabetes (T1D) came from genome-wide association studies that unequivocally connected genetic susceptibility to immune cell function. At the top of the susceptibility are genes involved in regulatory T-cell (Treg) function and development. The advances in epigenetic and transcriptional analyses have provided increasing evidence for Treg dysfunction in T1D. These are well supported by functional studies in mouse models and analysis of peripheral blood during T1D. For these reasons, Treg-based therapies are at the forefront of research and development and have a tangible probability to deliver a long-sought-after successful immune-targeted treatment for T1D. The current challenge in the field is whether we can directly assess Treg function at the tissue site or make informative interpretations based on peripheral data. Future studies focused on Treg function in pancreatic lymph nodes and pancreas could provide key insight into the ultimate mechanisms underlying Treg failure in T1D. In this Perspective we will provide an overview of current literature regarding Treg development and function in T1D and how this knowledge has been applied to Treg therapies.
    MeSH term(s) Animals ; Autoimmunity/physiology ; Diabetes Mellitus, Type 1/genetics ; Diabetes Mellitus, Type 1/immunology ; Diabetes Mellitus, Type 1/pathology ; Diabetes Mellitus, Type 1/therapy ; Endocrinology/methods ; Endocrinology/trends ; Humans ; Immune Tolerance/physiology ; Immunotherapy, Adoptive/methods ; Immunotherapy, Adoptive/trends ; Mice ; Molecular Targeted Therapy/methods ; Molecular Targeted Therapy/trends ; Pancreas/immunology ; Pancreas/metabolism ; Pancreas/pathology ; T-Lymphocytes, Regulatory/immunology ; T-Lymphocytes, Regulatory/metabolism ; T-Lymphocytes, Regulatory/physiology ; T-Lymphocytes, Regulatory/transplantation
    Language English
    Publishing date 2021-05-20
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 80085-5
    ISSN 1939-327X ; 0012-1797
    ISSN (online) 1939-327X
    ISSN 0012-1797
    DOI 10.2337/dbi18-0058
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: The Amphiregulin/EGFR axis has limited contribution in controlling autoimmune diabetes.

    Raugh, Arielle / Jing, Yi / Bettini, Matthew L / Bettini, Maria

    Research square

    2023  

    Abstract: Conventional immunosuppressive functions of CD4+Foxp3+ regulatory T cells (Tregs) in type 1 diabetes (T1D) pathogenesis have been well described, but whether Tregs have additional non-immunological functions supporting tissue homeostasis in pancreatic ... ...

    Abstract Conventional immunosuppressive functions of CD4+Foxp3+ regulatory T cells (Tregs) in type 1 diabetes (T1D) pathogenesis have been well described, but whether Tregs have additional non-immunological functions supporting tissue homeostasis in pancreatic islets is unknown. Within the last decade novel tissue repair functions have been ascribed to Tregs. One function is production of the epidermal growth factor receptor (EGFR) ligand, amphiregulin, which promotes tissue repair in response to inflammatory or mechanical tissue injury. Whether such pathways are engaged during autoimmune diabetes and promote tissue repair is undetermined. Previously, we observed upregulation of amphiregulin at the transcriptional level was associated with functional Treg populations in the non-obese diabetic (NOD) mouse model of T1D. We postulated that amphiregulin promoted islet tissue repair and slowed the progression of diabetes in NOD mice. Here, we report that islet-infiltrating Tregs have increased capacity to produce amphiregulin and both Tregs and beta cells express EGFR. Moreover, we show that amphiregulin can directly modulate mediators of endoplasmic reticulum (ER) stress in beta cells. Despite this, NOD amphiregulin deficient mice showed no acceleration of spontaneous autoimmune diabetes. Taken together, the data suggest that the ability for amphiregulin to affect the progression of autoimmune diabetes is limited.
    Language English
    Publishing date 2023-08-03
    Publishing country United States
    Document type Preprint
    DOI 10.21203/rs.3.rs-3204139/v1
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  4. Article ; Online: The amphiregulin/EGFR axis has limited contribution in controlling autoimmune diabetes.

    Raugh, Arielle / Jing, Yi / Bettini, Matthew L / Bettini, Maria

    Scientific reports

    2023  Volume 13, Issue 1, Page(s) 18653

    Abstract: Conventional immunosuppressive functions of ... ...

    Abstract Conventional immunosuppressive functions of CD4
    MeSH term(s) Animals ; Mice ; Amphiregulin/genetics ; Amphiregulin/metabolism ; Diabetes Mellitus, Type 1/metabolism ; ErbB Receptors/genetics ; ErbB Receptors/metabolism ; Islets of Langerhans/metabolism ; Mice, Inbred NOD ; T-Lymphocytes, Regulatory
    Chemical Substances Amphiregulin ; ErbB Receptors (EC 2.7.10.1) ; Areg protein, mouse ; EGFR protein, mouse (EC 2.7.10.1)
    Language English
    Publishing date 2023-10-30
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-45738-4
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  5. Article ; Online: Host-microbiota interactions shaping T-cell response and tolerance in type 1 diabetes.

    Majumdar, Shubhabrata / Lin, Yong / Bettini, Matthew L

    Frontiers in immunology

    2022  Volume 13, Page(s) 974178

    Abstract: Type-1 Diabetes (T1D) is a complex polygenic autoimmune disorder involving T-cell driven beta-cell destruction leading to hyperglycemia. There is no cure for T1D and patients rely on exogenous insulin administration for disease management. T1D is ... ...

    Abstract Type-1 Diabetes (T1D) is a complex polygenic autoimmune disorder involving T-cell driven beta-cell destruction leading to hyperglycemia. There is no cure for T1D and patients rely on exogenous insulin administration for disease management. T1D is associated with specific disease susceptible alleles. However, the predisposition to disease development is not solely predicted by them. This is best exemplified by the observation that a monozygotic twin has just a 35% chance of developing T1D after their twin's diagnosis. This makes a strong case for environmental triggers playing an important role in T1D incidence. Multiple studies indicate that commensal gut microbiota and environmental factors that alter their composition might exacerbate or protect against T1D onset. In this review, we discuss recent literature highlighting microbial species associated with T1D. We explore mechanistic studies which propose how some of these microbial species can modulate adaptive immune responses in T1D, with an emphasis on T-cell responses. We cover topics ranging from gut-thymus and gut-pancreas communication, microbial regulation of peripheral tolerance, to molecular mimicry of islet antigens by microbial peptides. In light of the accumulating evidence on commensal influences in neonatal thymocyte development, we also speculate on the link between molecular mimicry and thymic selection in the context of T1D pathogenesis. Finally, we explore how these observations could inform future therapeutic approaches in this disease.
    MeSH term(s) Autoimmune Diseases/complications ; Diabetes Mellitus, Type 1 ; Gastrointestinal Microbiome ; Humans ; Immune Tolerance ; Infant, Newborn ; Insulin
    Chemical Substances Insulin
    Language English
    Publishing date 2022-08-18
    Publishing country Switzerland
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural
    ZDB-ID 2606827-8
    ISSN 1664-3224 ; 1664-3224
    ISSN (online) 1664-3224
    ISSN 1664-3224
    DOI 10.3389/fimmu.2022.974178
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  6. Article: Increased TCR signaling in regulatory T cells is disengaged from TCR affinity.

    Jing, Yi / Kong, Yuelin / Allard, Denise / Liu, Baoyu / Kolawole, Elizabeth / Sprouse, Maran / Evavold, Brian / Bettini, Matthew / Bettini, Maria

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Foxp3+ regulatory T cells (Tregs) are capable suppressors of aberrant self-reactivity. However, TCR affinity and specificities that support Treg function, and how these compare to autoimmune T cells remain unresolved. In this study, we used antigen ... ...

    Abstract Foxp3+ regulatory T cells (Tregs) are capable suppressors of aberrant self-reactivity. However, TCR affinity and specificities that support Treg function, and how these compare to autoimmune T cells remain unresolved. In this study, we used antigen agnostic and epitope-focused analyses to compare TCR repertoires of regulatory and effector T cells that spontaneously infiltrate pancreatic islets of non-obese diabetic mice. We show that effector and regulatory T cell-derived TCRs possess similar wide-ranging reactivity for self-antigen. Treg-derived TCRs varied in their capacity to confer optimal protective function, and Treg suppressive capacity was in part determined by effector TCR affinity. Interestingly, when expressing the same TCR, Tregs showed higher Nur77-GFP expression than Teffs, suggesting Treg-intrinsic ability to compete for antigen. Our findings provide a new insight into TCR-dependent and independent mechanisms that regulate Treg function and indicate a TCR-intrinsic insufficiency in tissue-specific Tregs that may contribute to the pathogenesis of type 1 diabetes.
    Language English
    Publishing date 2023-01-24
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.01.17.523999
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  7. Article: Understanding Autoimmune Diabetes through the Prism of the Tri-Molecular Complex.

    Bettini, Matthew L / Bettini, Maria

    Frontiers in endocrinology

    2017  Volume 8, Page(s) 351

    Abstract: The strongest susceptibility allele for Type 1 Diabetes (T1D) is human leukocyte antigen (HLA), which supports a central role for T cells as the drivers of autoimmunity. However, the precise mechanisms that allow thymic escape and peripheral activation ... ...

    Abstract The strongest susceptibility allele for Type 1 Diabetes (T1D) is human leukocyte antigen (HLA), which supports a central role for T cells as the drivers of autoimmunity. However, the precise mechanisms that allow thymic escape and peripheral activation of beta cell antigen-specific T cells are still largely unknown. Studies performed with the non-obese diabetic (NOD) mouse have challenged several immunological dogmas, and have made the NOD mouse a key experimental system to study the steps of immunodysregulation that lead to autoimmune diabetes. The structural similarities between the NOD I-A
    Language English
    Publishing date 2017-12-14
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2592084-4
    ISSN 1664-2392
    ISSN 1664-2392
    DOI 10.3389/fendo.2017.00351
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  8. Article ; Online: Daring to learn from humanized mice.

    Paust, Silke / Bettini, Matthew

    Blood

    2015  Volume 125, Issue 25, Page(s) 3829–3831

    MeSH term(s) Animals ; Autoimmunity/immunology ; Disease Models, Animal ; Forkhead Transcription Factors/immunology ; Humans ; Immunologic Deficiency Syndromes/immunology
    Chemical Substances Forkhead Transcription Factors
    Language English
    Publishing date 2015-06-17
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 80069-7
    ISSN 1528-0020 ; 0006-4971
    ISSN (online) 1528-0020
    ISSN 0006-4971
    DOI 10.1182/blood-2015-04-639435
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  9. Article ; Online: Antibody-Mediated Targeting of a Hybrid Insulin Peptide Toward Neonatal Thymic Langerin-Positive Cells Enhances T-Cell Central Tolerance and Delays Autoimmune Diabetes.

    Lin, Yong / Perovanovic, Jelena / Kong, Yuelin / Igyarto, Botond Z / Zurawski, Sandra / Tantin, Dean / Zurawski, Gerard / Bettini, Maria / Bettini, Matthew L

    Diabetes

    2022  Volume 71, Issue 8, Page(s) 1735–1745

    Abstract: Thymic presentation of self-antigens is critical for establishing a functional yet self-tolerant T-cell population. Hybrid peptides formed through transpeptidation within pancreatic β-cell lysosomes have been proposed as a new class of autoantigens in ... ...

    Abstract Thymic presentation of self-antigens is critical for establishing a functional yet self-tolerant T-cell population. Hybrid peptides formed through transpeptidation within pancreatic β-cell lysosomes have been proposed as a new class of autoantigens in type 1 diabetes (T1D). While the production of hybrid peptides in the thymus has not been explored, due to the nature of their generation, it is thought to be highly unlikely. Therefore, hybrid peptide-reactive thymocytes may preferentially escape thymic selection and contribute significantly to T1D progression. Using an antibody-peptide conjugation system, we targeted the hybrid insulin peptide (HIP) 2.5HIP toward thymic resident Langerin-positive dendritic cells to enhance thymic presentation during the early neonatal period. Our results indicated that anti-Langerin-2.5HIP delivery can enhance T-cell central tolerance toward cognate thymocytes in NOD.BDC2.5 mice. Strikingly, a single dose treatment with anti-Langerin-2.5HIP during the neonatal period delayed diabetes onset in NOD mice, indicating the potential of antibody-mediated delivery of autoimmune neoantigens during early stages of life as a therapeutic option in the prevention of autoimmune diseases.
    MeSH term(s) Animals ; Antibodies ; Autoantigens ; Central Tolerance ; Diabetes Mellitus, Type 1 ; Insulin ; Insulin, Regular, Human ; Mice ; Mice, Inbred NOD ; Peptides ; Thymus Gland
    Chemical Substances Antibodies ; Autoantigens ; Insulin ; Insulin, Regular, Human ; Peptides
    Language English
    Publishing date 2022-07-13
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; 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/db21-1069
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  10. Article ; Online: A dormant T-cell population with autoimmune potential exhibits low self-reactivity and infiltrates islets in type 1 diabetes.

    Kong, Yuelin / Jing, Yi / Allard, Denise / Scavuzzo, Marissa A / Sprouse, Maran L / Borowiak, Malgorzata / Bettini, Matthew L / Bettini, Maria

    European journal of immunology

    2022  Volume 52, Issue 7, Page(s) 1158–1170

    Abstract: The contribution of low-affinity T cells to autoimmunity in the context of polyclonal T-cell responses is understudied due to the limitations in their capture by tetrameric reagents and low level of activation in response to antigenic stimulation. As a ... ...

    Abstract The contribution of low-affinity T cells to autoimmunity in the context of polyclonal T-cell responses is understudied due to the limitations in their capture by tetrameric reagents and low level of activation in response to antigenic stimulation. As a result, low-affinity T cells are often disregarded as nonantigen-specific cells irrelevant to the immune response. Our study aimed to assess how the level of self-antigen reactivity shapes T-cell lineage and effector responses in the context of spontaneous tissue-specific autoimmunity observed in NOD mice. Using multicolor flow cytometry in combination with Nur77
    MeSH term(s) Animals ; CD4-Positive T-Lymphocytes ; Diabetes Mellitus, Type 1 ; Mice ; Mice, Inbred NOD ; Mice, Transgenic ; Receptors, Antigen, T-Cell/genetics
    Chemical Substances Receptors, Antigen, T-Cell
    Language English
    Publishing date 2022-04-22
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Extramural
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.202149690
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