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      Two to Tango: Dialogue between Adaptive and Innate Immunity in Type 1 Diabetes

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          Abstract

          Type 1 diabetes mellitus (T1DM) is a long-term and chronic autoimmune disorder, in which the immune system attacks the pancreatic β-cells. Both adaptive and innate immune systems are involved in T1DM development. Both B-cells and T-cells, including CD4 + and CD8 + T-cells, as well as other T-cell subsets, could affect onset of autoimmunity. Furthermore, cells involved in innate immunity, including the macrophages, dendritic cells, and natural killer (NK) cells, could also accelerate or decelerate T1DM development. In this review, the crosstalk and function of immune cells in the pathogenesis of T1DM, as well as the corresponding therapeutic interventions, are discussed.

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          An Anti-CD3 Antibody, Teplizumab, in Relatives at Risk for Type 1 Diabetes

          Kevan C. Herold, Brian Bundy, S Alice Long … (2019)
          Type 1 diabetes is a chronic autoimmune disease that leads to destruction of insulin-producing beta cells and dependence on exogenous insulin for survival. Some interventions have delayed the loss of insulin production in patients with type 1 diabetes, but interventions that might affect clinical progression before diagnosis are needed.
          Article 0 comments Cited 332 times – based on 0 reviews     Review now
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            Crosstalk between neutrophils, B-1a cells and plasmacytoid dendritic cells initiates autoimmune diabetes.

            Agnès Lehuen, Lucie Beaudoin, Franck J. Barrat … (2012)
            Type 1 diabetes develops over many years and is characterized ultimately by the destruction of insulin-producing pancreatic beta cells by autoreactive T cells. Nonetheless, the role of innate cells in the initiation of this disease remains poorly understood. Here, we show that in young female nonobese diabetic mice, physiological beta cell death induces the recruitment and activation of B-1a cells, neutrophils and plasmacytoid dendritic cells (pDCs) to the pancreas. Activated B-1a cells secrete IgGs specific for double-stranded DNA. IgGs activate neutrophils to release DNA-binding cathelicidin-related antimicrobial peptide (CRAMP), which binds self DNA. Then, self DNA, DNA-specific IgG and CRAMP peptide activate pDCs through the Toll-like receptor 9-myeloid differentiation factor 88 pathway, leading to interferon-α production in pancreatic islets. We further demonstrate through the use of depleting treatments that B-1a cells, neutrophils and IFN-α-producing pDCs are required for the initiation of the diabetogenic T cell response and type 1 diabetes development. These findings reveal that an innate immune cell crosstalk takes place in the pancreas of young NOD mice and leads to the initiation of T1D.
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              Pro-inflammatory cytokines increase reactive oxygen species through mitochondria and NADPH oxidase in cultured RPE cells.

              Gerd Till, Susan Elner, Dongli Yang … (2007)
              Reactive oxygen species (ROS) generated during inflammation are believed to play critical roles in various ocular diseases. However, the underlying mechanisms remain poorly understood. We investigated if pro-inflammatory cytokines, tumor necrosis factor (TNF)-alpha, interleukin-1 beta (IL-1 beta), and interferon-gamma (IFN-gamma), induce ROS in human retinal pigment epithelial (RPE) cells. TNF-alpha, IL-1 beta and IFN-gamma increased both intracellular and extracellular ROS production in a time- and dose-dependent manner. Thenoyltrifluoroacetone (TTFA), an inhibitor of mitochondrial respiratory chain, blocked TNF-alpha- and IFN-gamma-, but not IL-1 beta-induced ROS, whereas other two mitochondrial respiratory chain inhibitors, rotenone and antimycin A, had no effect. NADPH oxidase inhibitor (diphenylene iodinium) abolished the ROS production induced by IL-1 beta or IFN-gamma, but not by TNF-alpha, whereas 6-aminonicotinamide (6AN), an inhibitor of the hexose monophosphate shunt (HMS), had no significant effects on the ROS induced by all three cytokines. ROS scavengers, pyrrolidinedithiocarbamate (PDTC) and N-acetyl-cysteine (NAC), reduced the levels of ROS induced by TNF-alpha, IL-1 beta and IFN-gamma (P<0.05). Collectively, these results demonstrate that TNF-alpha, IL-1 beta and IFN-gamma increase mitochondrial- and NADPH oxidase-generated ROS in human RPE cells.
              Article 0 comments Cited 135 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Guixia Wang:
                ORCID: https://orcid.org/0000-0001-8107-616X
                Journal
                Journal ID (nlm-ta): J Diabetes Res
                Journal ID (iso-abbrev): J Diabetes Res
                Journal ID (publisher-id): JDR
                Title: Journal of Diabetes Research
                Publisher: Hindawi
                ISSN (Print): 2314-6745
                ISSN (Electronic): 2314-6753
                Publication date Collection: 2020
                Publication date (Electronic): 30 July 2020
                Volume: 2020
                Electronic Location Identifier: 4106518
                Affiliations
                Department of Endocrinology and Metabolism, The First Hospital of Jilin University, Changchun, 130021 Jilin, China
                Author notes

                Academic Editor: Georgia Fousteri

                Author information
                https://orcid.org/0000-0002-1501-2181
                https://orcid.org/0000-0001-9939-8212
                https://orcid.org/0000-0002-7614-919X
                https://orcid.org/0000-0002-9463-5175
                https://orcid.org/0000-0003-3570-1918
                https://orcid.org/0000-0003-4198-5777
                https://orcid.org/0000-0001-8107-616X
                Article
                DOI: 10.1155/2020/4106518
                PMC ID: 7415089
                PubMed ID: 32802890
                SO-VID: b42f5c7e-a9fe-490c-a868-c57a15d6c03f
                Copyright © Copyright © 2020 Lin Sun et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 10 April 2020
                Date revision received : 18 June 2020
                Date accepted : 2 July 2020
                Categories
                Subject: Review Article

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