Immune cell crosstalk in type 1 diabetes

2010 ◽  
Vol 10 (7) ◽  
pp. 501-513 ◽  
Author(s):  
Agnès Lehuen ◽  
Julien Diana ◽  
Paola Zaccone ◽  
Anne Cooke
Keyword(s):  
Type 1 Diabetes ◽  
Immune Cell ◽  
Cell Crosstalk

Immunotherapy: Building a bridge to a cure for type 1 diabetes

Science ◽  
2021 ◽  
Vol 373 (6554) ◽  
pp. 510-516
Author(s):  
Jeffrey A. Bluestone ◽  
Jane H. Buckner ◽  
Kevan C. Herold
Keyword(s):  
Type 1 Diabetes ◽  
Immune Cell ◽  
Cell Types ◽  
Underlying Disease ◽  
Β Cells ◽  
Current State ◽  
Islet Inflammation ◽  
Genetic And Environmental Factors ◽  
Key Events

Type 1 diabetes (T1D) is an autoimmune disease in which T cells attack and destroy the insulin-producing β cells in the pancreatic islets. Genetic and environmental factors increase T1D risk by compromising immune homeostasis. Although the discovery and use of insulin have transformed T1D treatment, insulin therapy does not change the underlying disease or fully prevent complications. Over the past two decades, research has identified multiple immune cell types and soluble factors that destroy insulin-producing β cells. These insights into disease pathogenesis have enabled the development of therapies to prevent and modify T1D. In this review, we highlight the key events that initiate and sustain pancreatic islet inflammation in T1D, the current state of the immunological therapies, and their advantages for the treatment of T1D.

Korean red ginseng (Panax ginseng) ameliorates type 1 diabetes and restores immune cell compartments

2012 ◽  
Vol 144 (2) ◽  
pp. 225-233 ◽  
Author(s):  
Young Joo Hong ◽  
Nayoung Kim ◽  
Karim Lee ◽  
Chung Hee Sonn ◽  
Jung Eun Lee ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Panax Ginseng ◽  
Immune Cell ◽  
Red Ginseng ◽  
Korean Red Ginseng ◽  
Cell Compartments

Vitamin D and Omega-3 Polyunsaturated Fatty Acids in Type 1 Diabetes modulation

2022 ◽  
Vol 22 ◽  
Author(s):  
Thais Sibioni Berti Bastos ◽  
Tárcio Teodoro Braga ◽  
Mariana Rodrigues Davanso
Keyword(s):  
Fatty Acids ◽  
Vitamin D ◽  
Type 1 Diabetes ◽  
Polyunsaturated Fatty Acids ◽  
Immune Cell ◽  
Omega 3 ◽  
Β Cells ◽  
Potential Benefits ◽  
Chronic Autoimmune Disease

Background: Type 1 diabetes (T1D) is a chronic autoimmune disease that affects people globally. Usually developed during childhood, T1D is characterized by the destruction of pancreatic β-cells due to immune cell attack and the establishment of an inflammatory process. Objective: The study aimed to investigate the effects of vitamin D through its nuclear receptor and the ω-3 polyunsaturated fatty acids (PUFAs) through their lipid derivatives in T1D modulation. Both components exert anti-inflammatory activity and act directly on cells of the immune system, attenuating the destruction of insulin-producing cells. Furthermore, they lead to a better glycemic level, reducing the need for insulin and a normal immune state, such as C-peptide maintenance. Method: Presently, our review highlights the significant studies that evaluated the supplementation of vitamin D and ω-3 PUFAs in humans and animal models in the modulation of T1D. Conclusion: The data collected suggests that supplementation can provide potential benefits, mainly when done early in the diagnosis, since it reduces the need for insulin and the risk of complications generated by the disease.

scholarly journals Kinetics of immune cell responses in the multiple low‐dose streptozotocin mouse model of type 1 diabetes

2019 ◽  
Vol 1 (9) ◽  
pp. 538-549 ◽  
Author(s):  
Zhengkang Luo ◽  
Charlotte Soläng ◽  
Mariela Mejia‐Cordova ◽  
Lina Thorvaldson ◽  
Martin Blixt ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Mouse Model ◽  
Low Dose ◽  
Immune Cell ◽  
Cell Responses ◽  
Kinetics Of

scholarly journals Increased β-cell proliferation before immune cell invasion prevents progression of type 1 diabetes

2019 ◽  
Vol 1 (5) ◽  
pp. 509-518 ◽  
Author(s):  
Ercument Dirice ◽  
Sevim Kahraman ◽  
Dario F. De Jesus ◽  
Abdelfattah El Ouaamari ◽  
Giorgio Basile ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Type 1 Diabetes ◽  
Cell Invasion ◽  
Immune Cell ◽  
Β Cell

scholarly journals Blood Co-Circulating Extracellular microRNAs and Immune Cell Subsets Associate with Type 1 Diabetes Severity

2020 ◽  
Vol 21 (2) ◽  
pp. 477 ◽  
Author(s):  
Silvia Garavelli ◽  
Sara Bruzzaniti ◽  
Elena Tagliabue ◽  
Francesco Prattichizzo ◽  
Dario Di Silvestre ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
Immune Cell ◽  
Disease Onset ◽  
Cell Subset ◽  
Healthy Controls ◽  
Cell Frequency ◽  
Logistic Regression Models ◽  
Immune Cell Subsets ◽  
Diabetes Severity

Immune cell subsets and microRNAs have been independently proposed as type 1 diabetes (T1D) diagnostic and/or prognostic biomarkers. Here, we aimed to analyze the relationships between peripheral blood circulating immune cell subsets, plasmatic microRNAs, and T1D. Blood samples were obtained from both children with T1D at diagnosis and age-sex matched healthy controls. Then, immunophenotype assessed by flow cytometry was coupled with the quantification of 60 plasmatic microRNAs by quantitative RT-PCR. The associations between immune cell frequency, plasmatic microRNAs, and the parameters of pancreatic loss, glycemic control, and diabetic ketoacidosis were assessed by logistic regression models and correlation analyses. We found that the increase in specific plasmatic microRNAs was associated with T1D disease onset (let-7c-5p, let-7d-5p, let-7f-5p, let-7i-5p, miR-146a-5p, miR-423-3p, and miR-423-5p), serum C-peptide concentration (miR-142-5p and miR-29c-3p), glycated hemoglobin (miR-26a-5p and miR-223-3p) and the presence of ketoacidosis (miR-29c-3p) more strongly than the evaluated immune cell subset frequency. Some of these plasmatic microRNAs were shown to positively correlate with numbers of blood circulating B lymphocytes (miR-142-5p) and CD4+CD45RO+ (miR-146a-5p and miR-223-3p) and CD4+CD25+ cells (miR-423-3p and miR-223-3p) in children with T1D but not in healthy controls, suggesting a disease-specific microRNA association with immune dysregulation in T1D. In conclusion, our results suggest that, while blood co-circulating extracellular microRNAs and immune cell subsets may be biologically linked, microRNAs may better provide powerful information about T1D onset and severity.

scholarly journals An HLA-Transgenic Mouse Model of Type 1 Diabetes That Incorporates the Reduced but Not Abolished Thymic Insulin Expression Seen in Patients

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Jeffrey Babad ◽  
Riyasat Ali ◽  
Jennifer Schloss ◽  
Teresa P. DiLorenzo
Keyword(s):  
Type 1 Diabetes ◽  
T Cell ◽  
Beta Cells ◽  
Immune Cell ◽  
Regulatory Region ◽  
Islet Autoimmunity ◽  
Positive Type ◽  
Insulin Expression ◽  
Pancreatic Islet Beta Cells

Type 1 diabetes (T1D) is an autoimmune disease characterized by T cell-mediated destruction of the pancreatic islet beta cells. Multiple genetic loci contribute to disease susceptibility in humans, with the most responsible locus being the major histocompatibility complex (MHC). Certain MHC alleles are predisposing, including the common HLA-A∗02:01. After the MHC, the locus conferring the strongest susceptibility to T1D is the regulatory region of the insulin gene, and alleles associated with reduced thymic insulin expression are predisposing. Mice express two insulin genes,Ins1andIns2. While both are expressed in beta cells, onlyIns2is expressed in the thymus. We have developed an HLA-A∗02:01-transgenic NOD-based T1D model that is heterozygous for a functionalIns2gene. These mice exhibit reduced thymic insulin expression and accelerated disease in both genders. Immune cell populations are not grossly altered, and the mice exhibit typical signs of islet autoimmunity, including CD8 T cell responses to beta cell peptides also targeted in HLA-A∗02:01-positive type 1 diabetes patients. This model should find utility as a tool to uncover the mechanisms underlying the association between reduced thymic insulin expression and T1D in humans and aid in preclinical studies to evaluate insulin-targeted immunotherapies for the disease.

Sign in / Sign up

Export Citation Format

Share Document