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Autoimmune CD8+ T cells in type 1 diabetes: from single-cell RNA sequencing to T-cell receptor redirection.
- Source :
-
Frontiers in endocrinology [Front Endocrinol (Lausanne)] 2024 May 10; Vol. 15, pp. 1377322. Date of Electronic Publication: 2024 May 10 (Print Publication: 2024). - Publication Year :
- 2024
-
Abstract
- Type 1 diabetes (T1D) is an organ-specific autoimmune disease caused by pancreatic β cell destruction and mediated primarily by autoreactive CD8+ T cells. It has been shown that only a small number of stem cell-like β cell-specific CD8+ T cells are needed to convert normal mice into T1D mice; thus, it is likely that T1D can be cured or significantly improved by modulating or altering self-reactive CD8+ T cells. However, stem cell-type, effector and exhausted CD8+ T cells play intricate and important roles in T1D. The highly diverse T-cell receptors (TCRs) also make precise and stable targeted therapy more difficult. Therefore, this review will investigate the mechanisms of autoimmune CD8+ T cells and TCRs in T1D, as well as the related single-cell RNA sequencing (ScRNA-Seq), CRISPR/Cas9, chimeric antigen receptor T-cell (CAR-T) and T-cell receptor-gene engineered T cells (TCR-T), for a detailed and clear overview. This review highlights that targeting CD8+ T cells and their TCRs may be a potential strategy for predicting or treating T1D.<br />Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.<br /> (Copyright © 2024 Yang, Zhang, Ding, Li, Zhang and Zou.)
- Subjects :
- Humans
Animals
Sequence Analysis, RNA methods
Insulin-Secreting Cells immunology
Insulin-Secreting Cells metabolism
Autoimmunity
Mice
Diabetes Mellitus, Type 1 immunology
Diabetes Mellitus, Type 1 genetics
CD8-Positive T-Lymphocytes immunology
Receptors, Antigen, T-Cell immunology
Receptors, Antigen, T-Cell genetics
Receptors, Antigen, T-Cell metabolism
Single-Cell Analysis methods
Subjects
Details
- Language :
- English
- ISSN :
- 1664-2392
- Volume :
- 15
- Database :
- MEDLINE
- Journal :
- Frontiers in endocrinology
- Publication Type :
- Academic Journal
- Accession number :
- 38800484
- Full Text :
- https://doi.org/10.3389/fendo.2024.1377322