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Biomolecules
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Immune and Pancreatic β Cell Signalling and Cross-Talk in the...
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Immune and Pancreatic β Cell Signalling and Cross-Talk in the Pathogenesis of Type 1 Diabetes

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (15 August 2021) | Viewed by 11133

Special Issue Editor

Dr. Peter J. Thompson

E-Mail Website
Guest Editor
Department of Physiology and Pathophysiology, Rady Faculty of Health Sciences, University of Manitoba, Winnipeg, MB, Canada
Interests: pancreatic islets; islet autoimmunity; cellular stress responses; molecular mecanisms of disease; small-molecule drugs; glucose metabolism; immunometabolism

Special Issue Information

Dear Colleagues,

Type 1 Diabetes (T1D) is a chronic metabolic disease of insulin deficiency due to autoimmune destruction of pancreatic beta cells. Although the role of beta cell autoimmunity in this disease has been recognized for decades, many major questions remain surrounding the molecular mechanisms that govern T1D development, the autoimmune process, and the role of beta cells themselves in the disease.

Recent years have seen advances in our understanding of the wide variety of molecular factors such as cytokines, chemokines, proteases, growth factors, cell surface receptors, microRNAs, exosomes, metabolites, and hormones, involved in the signalling between beta cells and various immune cells in T1D. Despite this growth in this field, there are major gaps not only in our understanding of fundamental disease mechanisms but also in how these mechanisms translate from cellular and animal models to humans.

The current Special Issue invites original research and review submissions focused on specific molecules or other factors (e.g., exosomes) and their roles in mediating signalling between immune cells and islets/beta cells in the pathogenesis of T1D. Mechanistic studies using human models, specimens, or human stem-cell-derived beta cells are especially encouraged. Submissions are also invited that demonstrate novel therapeutics targeting the immune system and/or beta cells and their application to the prevention and/or treatment of T1D.

Sincerely,

Dr. Peter J. Thompson
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Biomolecules is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • pancreatic beta cells
  • islet autoimmunity
  • molecular mechanisms of disease
  • disease heterogeneity
  • therapeutics

Published Papers (3 papers)

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Research

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25 pages, 7111 KiB  
Article
Islet Dysfunction in a Novel Transgenic Model of T Cell Insulitis
by Emily Esakov, Neha Nandedkar-Kulkarni, Ali G. Al-Dieri, Hannah Hafner, Brigid Gregg and Marcia F. McInerney
Biomolecules 2021, 11(4), 552; https://doi.org/10.3390/biom11040552 - 09 Apr 2021
Cited by 1 | Viewed by 2242
Abstract
The newly established CD3FLAG-mIR transgenic mouse model on a C57Bl/6 background has a FLAG tag on the mouse Insulin Receptor (mIR), specifically on T cells, as the FLAG-tagged mIR gene was engineered behind CD3 promoter and enhancer. The IR is a chemotactic molecule [...] Read more.
The newly established CD3FLAG-mIR transgenic mouse model on a C57Bl/6 background has a FLAG tag on the mouse Insulin Receptor (mIR), specifically on T cells, as the FLAG-tagged mIR gene was engineered behind CD3 promoter and enhancer. The IR is a chemotactic molecule for insulin and the Flag-tagged mIR T cells in the BL/6-CD3FLAGmIR transgenic mice can migrate into the pancreas, as shown by immunofluorescent staining. While the transgenic mice do not become diabetic, there are phenotypic and metabolic changes in the islets. The transgenic islets become enlarged and disorganized by 15 weeks and those phenotypes continue out to 35 weeks of age. We examined the islets by RT-PCR for cell markers, ER stress markers, beta cell proliferation markers, and cytokines, as well as measuring serum insulin and insulin content in the pancreas at 15, 25, and 35 weeks of age. In transgenic mice, insulin in serum was increased at 15 weeks of age and glucose intolerance developed by 25 weeks of age. Passage of transgenic spleen cells into C57Bl/6 RAG−/− mice resulted in enlarged and disorganized islets with T infiltration by 4 to 5 weeks post-transfer, replicating the transgenic mouse studies. Therefore, migration of non-antigen-specific T cells into islets has ramifications for islet organization and function. Full article
(This article belongs to the Special Issue Immune and Pancreatic β Cell Signalling and Cross-Talk in the Pathogenesis of Type 1 Diabetes)
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Review

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10 pages, 796 KiB  
Review
Inherent Beta Cell Dysfunction Contributes to Autoimmune Susceptibility
by Yong Kyung Kim, Lori Sussel and Howard W. Davidson
Biomolecules 2021, 11(4), 512; https://doi.org/10.3390/biom11040512 - 30 Mar 2021
Cited by 6 | Viewed by 2897
Abstract
The pancreatic beta cell is a highly specialized cell type whose primary function is to secrete insulin in response to nutrients to maintain glucose homeostasis in the body. As such, the beta cell has developed unique metabolic characteristics to achieve functionality; in healthy [...] Read more.
The pancreatic beta cell is a highly specialized cell type whose primary function is to secrete insulin in response to nutrients to maintain glucose homeostasis in the body. As such, the beta cell has developed unique metabolic characteristics to achieve functionality; in healthy beta cells, the majority of glucose-derived carbons are oxidized and enter the mitochondria in the form of pyruvate. The pyruvate is subsequently metabolized to induce mitochondrial ATP and trigger the downstream insulin secretion response. Thus, in beta cells, mitochondria play a pivotal role in regulating glucose stimulated insulin secretion (GSIS). In type 2 diabetes (T2D), mitochondrial impairment has been shown to play an important role in beta cell dysfunction and loss. In type 1 diabetes (T1D), autoimmunity is the primary trigger of beta cell loss; however, there is accumulating evidence that intrinsic mitochondrial defects could contribute to beta cell susceptibility during proinflammatory conditions. Furthermore, there is speculation that dysfunctional mitochondrial responses could contribute to the formation of autoantigens. In this review, we provide an overview of mitochondrial function in the beta cells, and discuss potential mechanisms by which mitochondrial dysfunction may contribute to T1D pathogenesis. Full article
(This article belongs to the Special Issue Immune and Pancreatic β Cell Signalling and Cross-Talk in the Pathogenesis of Type 1 Diabetes)
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20 pages, 694 KiB  
Review
Beta Cell Therapies for Preventing Type 1 Diabetes: From Bench to Bedside
by Gabriel Brawerman and Peter J. Thompson
Biomolecules 2020, 10(12), 1681; https://doi.org/10.3390/biom10121681 - 16 Dec 2020
Cited by 17 | Viewed by 5217
Abstract
Type 1 diabetes (T1D) is a chronic metabolic disease characterized by insulin deficiency, generally resulting from progressive autoimmune-mediated destruction of pancreatic beta cells. While the phenomenon of beta cell autoimmunity continues to be an active area of investigation, recent evidence suggests that beta [...] Read more.
Type 1 diabetes (T1D) is a chronic metabolic disease characterized by insulin deficiency, generally resulting from progressive autoimmune-mediated destruction of pancreatic beta cells. While the phenomenon of beta cell autoimmunity continues to be an active area of investigation, recent evidence suggests that beta cell stress responses are also important contributors to disease onset. Here we review the pathways driving different kinds of beta cell dysfunction and their respective therapeutic targets in the prevention of T1D. We discuss opportunities and important open questions around the effectiveness of beta cell therapies and challenges for clinical utility. We further evaluate ways in which beta cell drug therapy could be combined with immunotherapy for preventing T1D in light of our growing appreciation of disease heterogeneity and patient endotypes. Ultimately, the emergence of pharmacologic beta cell therapies for T1D have armed us with new tools and closing the knowledge gaps in T1D etiology will be essential for maximizing the potential of these approaches. Full article
(This article belongs to the Special Issue Immune and Pancreatic β Cell Signalling and Cross-Talk in the Pathogenesis of Type 1 Diabetes)
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