The detection of pathogens by the immune system is facilitated through various cellular interactions and molecules, including pattern recognition receptors that activate signaling pathways in response to the pathogen. Among the most studied receptors are Toll-like receptors, which are activated upon ligand recognition and are considered the first event in innate immunity. The transcriptional response of TLRs in infected cells is modified by pathogens, where miRNAs, which are post-transcriptional regulators of gene expression, play a role. We review some bacteria that alter the signaling cascade of extracellular TLRs and the co-participation of miRNAs, most of which are analyzed downstream, and a very low percentage act as ligands of the TLRs. There is an increase in knowledge of the regulation of miRNAs by bacteria; however, the functional complexity of miRNAs has hindered progress in utilizing them as biomarkers or for therapeutic purposes.

Regulatory cells are critical for maintaining immune homeostasis in the central nervous system. Regulatory cell populations have been reported to control neuroinflammation in neurodegenerative conditions like Parkinson’s disease, multiple sclerosis, myasthenia gravis, encephalomyelitis, and Alzheimer’s disease by protecting neurons through different mechanisms, including the production of cytokines such as IL-10 and TGF-β, promoting the expression of inhibitory receptors (PD1, TIM3, LAG3), and inducing tolerance through cell-cell interactions by CTLA-4. Various phenotypes of CD4+ and CD8+ regulatory T cells, Bregs, MDCS, and tolDCs have been described and, despite the great interest in their function, few studies have focused on elucidating their role in neurodegenerative diseases. Therefore, this review aims to describe the mechanisms of regulation and suppression of effector cells in neurodegenerative diseases. The study of these mechanisms has led to the development of therapeutic approaches targeting molecules with suppressive or regulatory activity in severe neurological disorders.