The growing interest in microbiota-epigenetics-immune system research stems from the understanding that microbiota, a group of micro-organisms colonized in the human body, can influence the gene expression through epigenetic mechanisms and interaction with the immune system. Epigenetics refers to changes in gene activity that are not caused by the alteration in the DNA sequence itself. The clinical significance of this research lies in the potential to develop new therapies for diseases linked to the imbalance of these microbial species (dysbiosis), such as cancer and neurodegenerative diseases. The intricate interaction between microbiota and epigenetics involves the production of metabolites and signalling molecules that can impact our health by influencing immune responses, metabolism and inflammation. Understanding these interactions could lead to novel therapeutic strategies targeting microbiota-epigenetic pathways to improve health outcomes. In this context, we aim to review and emphasize the current knowledge and key concepts that link the microbiota to epigenetics and immune system function, exploring their relevance to the development and maintenance of homeostasis and susceptibility to different diseases later in life. We aim to elucidate key concepts concerning the interactions and potential effects among the human gut microbiota, epigenetics, the immune system and ageing diseases linked to dysbiosis.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1099/jmm.0.001921 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Anti-correlation of KLRG1 and PD-1 expression in human tumor CD8 T cells.
Oncotarget
January 2025
Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
Recently, combination checkpoint therapy of cancer has been recognized as producing additive as opposed to synergistic benefit due in part to positively correlated effects. The potential for uncorrelated or negatively correlated therapies to produce true synergistic benefits has been noted. Whereas the inhibitory receptors PD-1, CTLA-4, TIM-3, LAG-3, and TIGIT have been collectively characterized as exhaustion receptors, another inhibitory receptor KLRG1 was historically characterized as a senescent receptor and received relatively little attention as a potential checkpoint inhibitor target.
View Article and Find Full Text PDFCharacterization of Tumor Antigens from Multi-omics Data: Computational Approaches and Resources.
Genomics Proteomics Bioinformatics
January 2025
Center for Epigenetics and Disease Prevention, Institute of Biosciences and Technology, Texas A&M University, Houston, TX 77030, USA.
Tumor-specific antigens, also known as neoantigens, have potential utility in anti-cancer immunotherapy, including immune checkpoint blockade (ICB), neoantigen-specific T cell receptor-engineered T (TCR-T), chimeric antigen receptor T (CAR-T), and therapeutic cancer vaccines (TCVs). After recognizing presented neoantigens, the immune system becomes activated and triggers the death of tumor cells. Neoantigens may be derived from multiple origins, including somatic mutations (single nucleotide variants, insertion/deletions, and gene fusions), circular RNAs, alternative splicing, RNA editing, and polymorphic microbiome.
View Article and Find Full Text PDFThe immune exhaustion paradox: activated functionality during chronic bacterial infections.
J Infect Dev Ctries
December 2024
Department of Immunology, School of Medicine and Dr. Jose Eleuterio Gonzalez University Hospital, Universidad Autónoma de Nuevo León, Monterrey, Mexico.
Co-inhibitory molecules, such as cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) and programmed cell death protein 1 (PD-1), known as immune checkpoints, regulate the activity of T and myeloid cells during chronic viral infections and are well-established for their roles in cancer therapy. However, their involvement in chronic bacterial infections, particularly those caused by pathogens endemic to developing countries, such as Mycobacterium tuberculosis (Mtb), remains incompletely understood. Cytokine microenvironment determines the expression of co-inhibitory molecules in tuberculosis: Results indicate that the cytokine IL-12, in the presence of Mtb antigens, can enhance the expression of co-inhibitory molecules while preserving the effector and memory phenotypes of CD4+ T cells.
View Article and Find Full Text PDFcirc_0075829 regulates ferroptosis and immune escape in colon cancer cells through the miR-330-5p/TCF4 axis.
Neoplasma
December 2024
Department of Gastrointestinal Surgery, Renmin Hospital of Wuhan University, Wuchang, Wuhan, Hubei, China.
Many lines of evidence suggest that circular RNAs (circRNAs) are closely associated with the occurrence and progression of colon cancer. The objective of this study was to investigate the regulatory effects and mechanisms of circ_0075829 on ferroptosis and immune escape in colon cancer. We utilized colon cancer cell lines and a xenograft mouse model to analyze the function of circ_0075829 in vitro and in vivo.
View Article and Find Full Text PDFPan-cancer analysis and single-cell analysis identifies the CENPN as a biomarker for survival prognosis and immunotherapy.
Discov Oncol
January 2025
Department of Oncology, Fuyang Hospital of Anhui Medical University, Fuyang, 236000, China.
Background: Centromere protein N (CENPN), located on chromosome 16q23.2, encodes vital nucleosome-associated complexes that are essential for dynamic assembly processes. CENPN plays a pivotal role in regulating cell proliferation and cell cycle progression by influencing mitotic events.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!