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Updated: Jun 6, 2025

Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
An overview on the interaction between non-coding RNAs and CTLA-4 gene in human diseases
Amir Ebrahimi1, Tahereh Barati1, Zohreh Mirzaei1
1Department of Medical Genetics, Faculty of Medicine, Tabriz University of Medical Genetics, Tabriz, Iran.
Abstract:
Cytotoxic T lymphocyte antigen 4 (CTLA-4), in conjunction with PD-1 and CD28, plays a pivotal role in the modulation of T-cell activation. Specifically, CTLA-4 exerts its influence by impeding the generation of IL-2 and the proliferation of T cells. CTLA-4, being a receptor with a high affinity, engages in competitive binding with CD28 for the interaction with primary T-cell activator molecules, specifically CD80 and CD86. The appropriate functioning of T-cell activation is contingent upon maintaining a precise equilibrium between CTLA-4 and CD28. Consequently, any disruption in the expression of CTLA-4 significantly enhances the risk for a range of severe ailments, such as cancer, infectious diseases, allergies, and notably autoimmune diseases. The significance of epigenetic regulation of CTLA-4, particularly through non-coding RNAs (ncRNAs) such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), has considerable weight within this particular framework. To date, there have been associations shown between various abnormalities in the expression of ncRNAs that regulate CTLA-4 and clinicopathological characteristics. Nevertheless, it is evident that there is a lack of a comprehensive investigation. Hence, the present work was undertaken to summarize the existing research on the epigenetic control of CTLA-4, with a primary emphasis on elucidating the regulatory procedures, biological processes, and clinical applications in human diseases. The objective of this review is to acquire a thorough comprehension of the relationship between RNA/lncRNA/miRNA/mRNA (CTLA-4) and its role in the progression of diverse human disorders.
Insights
Epigenetic regulation of Cytotoxic T lymphocyte antigen 4 (CTLA-4) by non-coding RNAs (ncRNAs) is crucial for T-cell activation and preventing diseases. This review summarizes ncRNA regulation of CTLA-4 in human disorders.
Area of Science:
- Immunology
- Epigenetics
- Molecular Biology
Background:
- Cytotoxic T lymphocyte antigen 4 (CTLA-4) is a key regulator of T-cell activation, influencing IL-2 production and T-cell proliferation.
- Dysregulation of CTLA-4 expression is linked to severe conditions including cancer, infectious diseases, allergies, and autoimmune diseases.
- Non-coding RNAs (ncRNAs), such as microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs), are significant epigenetic regulators of CTLA-4.
Purpose of the Study:
- To review and summarize current research on the epigenetic control of CTLA-4.
- To elucidate the regulatory mechanisms, biological processes, and clinical applications of ncRNA-mediated CTLA-4 regulation in human diseases.
- To provide a comprehensive understanding of the CTLA-4/ncRNA/mRNA axis in disease pathogenesis.
Main Methods:
- Literature review and synthesis of existing research.
- Analysis of studies investigating ncRNA regulation of CTLA-4.
- Examination of associations between CTLA-4-regulating ncRNAs and clinicopathological characteristics.
Main Results:
- Abnormalities in ncRNAs regulating CTLA-4 have been associated with various clinicopathological features.
- A significant gap exists in comprehensive investigations of CTLA-4 epigenetic regulation by ncRNAs.
- Existing data highlight the critical role of ncRNAs in modulating CTLA-4 expression and its downstream effects.
Conclusions:
- Epigenetic regulation, particularly by ncRNAs, plays a vital role in maintaining CTLA-4 homeostasis.
- Understanding CTLA-4 epigenetic regulation by ncRNAs is essential for comprehending its role in diverse human diseases.
- Further comprehensive research is needed to fully elucidate the clinical implications of CTLA-4-targeting ncRNAs.
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