Type 1 diabetes mellitus (T1DM), a complex chronic disease with an intricate etiology and pathogenesis, involves the recognition of self-antigens by pancreatic islet autoantigen-specific T cells and plays crucial roles in both early- and late-stage destruction of beta cells, thus impacting disease progression. Antigen-specific T cells regulate and execute immune responses by recognizing particular antigens, playing broad roles in the treatment of various diseases. Immunotherapy targeting antigen-specific T cells holds promising potential as a targeted treatment approach. This review outlines the pathogenesis of diabetes, emphasizing the pivotal role of pancreatic islet autoantigen-specific T cells in the progression and treatment of T1DM. Exploring this avenue in research holds promise for identifying novel therapeutic targets for effectively managing diabetes.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11458421 | PMC |
| http://dx.doi.org/10.3389/fimmu.2024.1462384 | DOI Listing |
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The role of islet autoantigen-specific T cells in the onset and treatment of type 1 diabetes mellitus.
Front Immunol
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Sinopharm Dongfeng General Hospital (Hubei Clinical Research Center of Hypertension), School of Basic Medical Sciences, Hubei University of Medicine, Shiyan, China.
Type 1 diabetes mellitus (T1DM), a complex chronic disease with an intricate etiology and pathogenesis, involves the recognition of self-antigens by pancreatic islet autoantigen-specific T cells and plays crucial roles in both early- and late-stage destruction of beta cells, thus impacting disease progression. Antigen-specific T cells regulate and execute immune responses by recognizing particular antigens, playing broad roles in the treatment of various diseases. Immunotherapy targeting antigen-specific T cells holds promising potential as a targeted treatment approach.
View Article and Find Full Text PDFFactors Governing B Cell Recognition of Autoantigen and Function in Type 1 Diabetes.
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April 2024
Department of Pathology, Microbiology and Immunology, Vanderbilt University Medical Center, Nashville, TN 37232, USA.
Islet autoantibodies predict type 1 diabetes (T1D) but can be transient in murine and human T1D and are not thought to be directly pathogenic. Rather, these autoantibodies signal B cell activity as antigen-presenting cells (APCs) that present islet autoantigen to diabetogenic T cells to promote T1D pathogenesis. Disrupting B cell APC function prevents T1D in mouse models and has shown promise in clinical trials.
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Department of Immunology and Theranostics, Duarte, USA; Arthur Riggs Diabetes & Metabolism Research Institute, City of Hope, Duarte, California, USA. Electronic address:
CD6 is a glycoprotein expressed on CD4 and CD8 T cells involved in immunoregulation. CD318 has been identified as a CD6 ligand. The role of CD318 in T cell immunity is restricted as it has only been investigated in a few mice autoimmune models but not in human diseases.
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Institute for Pharmacology and Toxicology Pharmazentrum Frankfurt / ZAFES, Goethe University Frankfurt, Frankfurt am Main, Germany. Electronic address:
Article Synopsis
- Type 1 diabetes happens when the body's immune system mistakenly attacks and destroys insulin-producing cells in the pancreas.
- Treatment mainly involves giving insulin from outside the body, and there are not many other therapies that can target the immune system directly.
- In a study with mice, researchers found specific proteins and genes related to inflammation in the pancreas that could help with new treatments, especially focusing on how certain chemicals called chemokines make immune cells move around and cause problems.
HLA-DQ8 Supports Development of Insulitis Mediated by Insulin-Reactive Human TCR-Transgenic T Cells in Nonobese Diabetic Mice.
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The Jackson Laboratory, Bar Harbor, ME.
In an effort to improve HLA-"humanized" mouse models for type 1 diabetes (T1D) therapy development, we previously generated directly in the NOD strain CRISPR/Cas9-mediated deletions of various combinations of murine MHC genes. These new models improved upon previously available platforms by retaining β2-microglobulin functionality in FcRn and nonclassical MHC class I formation. As proof of concept, we generated H2-Db/H2-Kd double knockout NOD mice expressing human HLA-A*0201 or HLA-B*3906 class I variants that both supported autoreactive diabetogenic CD8+ T cell responses.
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