Nucleic acid recognition by toll-like receptor 9 (TLR9) initiates signaling pathways that regulate the production of proinflammatory cytokines or type I interferons, as well as many other molecules required to initialize the immune response. The use of synthetic oligodeoxynucleotides (ODNs) has been crucial to emulate the recognition of DNA sequences by TLR9. Furthermore, ODN administration to mice has shown to confer protection against a wide range of viral, bacterial, and parasitic pathogens. In contrast, oncogenic DNA viruses like hepatitis B virus, Epstein–Barr virus, and human papilloma virus inhibit TLR9 expression, thus contributing to the establishment of chronic viral infections. In this review, we will focus on TLR9 signals initiated by ODN recognition, on the inhibition of TLR9 expression mediated by DNA oncogenic viruses, and on TLR9 expression as a relevant event in the progression to cancer, considering other functions of this receptor, aside from viral recognition.

Helicobacter pylori infection is recognized as the main risk factor for gastric cancer (GC), the fifth most common neoplasia worldwide. H. pylori interacts with the immune system, disrupting the cytokine network and inducing chronic inflammation. This work aimed to evaluate the association between single nucleotide polymorphisms (SNPs) in selected cytokine gene promoters and GC. The study included 359 subjects, 125 GC patients, 109 intestinal metaplasia (IM) patients and 125 asymptomatic controls. DNA was extracted from white blood cells and nine SNPs in cytokine gene promoters were genotyped using predesigned 5′-endonulease assays. The association of the SNPs with IM and GC was evaluated using multinomial regression models. Both genotypes, TC (OR = 0.51, 95% CI = 0.27–0.98) and TT (OR = 0.42, 95% CI = 0.20–0.91) in the locus − 509 of the TGF-β promoter were significantly associated with GC. The TT genotype in the locus − 819 of the IL-10 promoter was also significantly associated with GC (OR = 0.37, 95% CI = 0.17–0.81). No significant association was found with SNPs IL-4 –590 T/C (rs1800629), IL-6 –573G/C (rs1800796), IL-10 –592C/A (rs1800872), IL-10 –1082A/G (rs1800896), and, IFN-γ –1615C/T (rs2069705). SNPs in TGFβ (− 509 C/T, rs1800469) and IL-10 (− 819 C/T, rs1800871) promoters were associated with a lower risk for GC in a Mexican population.

This review examines the evolutionary trajectory and functional versatility of RNA, beginning with its proposed involvement in the origin of life and culminating in its current application in therapeutic strategies. We explored the complexity of the transcriptome, splicing mechanisms, and the regulatory functions of non-coding RNAs, especially microRNAs. The processes underlying microRNA biogenesis and activity are discussed in the context of their potential as therapeutic tools. Advances in RNA-based technologies have been further illustrated by the development of mRNA vaccines, representing a significant breakthrough in biomedical innovation. Additionally, we explored the growing field of epitranscriptomics—chemical modifications to RNA that modulate its stability, translation, and function—by analyzing the roles of modification enzymes known as writers, erasers, and readers. Focus is given to how these alterations influence immune reactions and guide the strategic development of future modified mRNA vaccines. Collectively, these advances underscore RNA’s multifaceted roles and its transformative potential in the biological and medical sciences.