Abstract
The concept of “trained innate immunity” is understood as the ability of innate immune cells to remember invading agents and to respond nonspecifically to reinfection with increased strength. Trained immunity is orchestrated by epigenetic modifications leading to changes in gene expression and cell physiology. Although this phenomenon was originally seen mainly as a beneficial effect, since it confers broad immunological protection, enhanced immune response of reprogrammed innate immune cells might result in the development or persistence of chronic metabolic, autoimmune or neuroinfalmmatory disorders. This paper overviews several examples where the induction of trained immunity may be essential in the development of diseases characterized by flawed innate immune response.
Highlights
It was believed that the innate immunity arm of the immune system was less sophisticated than the adaptive immunity arm
Studies conducted with the use of bovine and human aortic endothelial cells have shown their epigenetic reprogramming through increased H3K4 monomethylation at the NF-κB promoter, which results in the production of reactive oxygen species (ROS) and upregulation of p65, MCP-1 and VCAM-1
Recent large-scale genome-wide association studies (GWAS) have proved that the risk of developing late-onset Alzheimer’s disease (AD) is significantly associated with rare variants of innate immune receptors expressed on the microglia surface, such as CD33 and the triggering receptor expressed on myeloid cells 2 (TREM2)
Summary
It was believed that the innate immunity arm of the immune system was less sophisticated than the adaptive immunity arm. The primary criterion for such an assessment was the ability of B and T cells, which represent the adaptive immunity, to mount immunological memory [1]. Studies carried out over the past few decades have shown that certain adaptations connected with innate immune cells (monocyte/macrophages, NK (Natural Killer) cells) are responsible for the nonspecific effects of vaccination [5,6]. In 2011, Netea et al proposed the term “trained immunity” to describe the ability of innate immune cells to nonspecifically adapt after primary stimulation (e.g., infection or vaccine) and remain at the increased “standby status” for a significant amount of time to be protective against secondary challenge, involving pathogens unrelated to the priming stimuli [7]. An increasing number of studies provide evidence that epigenetic reprogramming leading to functional and transcriptional changes in the innate immune cells may play a significant role in the maintenance of different disorders
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