The adaptive immune system can develop antigen-specific memory T cells and B cells that have previously encountered and responded to their cognate antigen. Recently, it was discovered that innate immune cells are also capable of developing an innate immune memory (trained immunity) when exposed to certain inflammatory stimuli. Innate immune cells such as monocytes, macrophages, dendritic cells, and natural killer (NK) cells, conditional innate immune cells such as endothelial cells and vascular smooth muscle cells, and non-immune cells were shown to develop trained immunity by undergoing functional reprogramming when exposed to inflammatory stimuli. These stimuli elicit elevated and potentially prolonged/chronic responses to subsequent inflammatory challenges. This long-term reprogramming depends on the rewiring of cell metabolism and epigenetic processes. For example, a few histone modifications have been reported to regulate trained immunity including histone 3 lysine 4 methylation (H3K4me1), H3K4 dimethylation (H3K4me2), H3K4 trimethylation (H3K4me3), H3K9me2, H3K27me3, H3K4 acetylation (H3K4Ac), H3K14Ac, H3K27Ac.Since the field is at the beginning stage, many important questions remain unaddressed. We welcome the submission of Original Research, Systematic Review, Methods. Review, Mini Review, Hypothesis & Theory, Perspective, Clinical Trial, Case Report, Classification, General Commentary, Opinion and Technology & Code focusing on, but not limited to, the following topics:
1. How oxidative stresses regulate trained immunity in pathophysiological conditions
2. How epigenetic modifications such as histone methylations and acetylations regulate trained immunity.
3. How non-coding RNAs regulate trained immunity
The novel insights gained by addressing these questions may lead to identification of new chronic disease risk factors that mediate trained immunity pathways and may potentiate identification of novel therapeutic targets for the treatment of chronic inflammation, and cancers.
The adaptive immune system can develop antigen-specific memory T cells and B cells that have previously encountered and responded to their cognate antigen. Recently, it was discovered that innate immune cells are also capable of developing an innate immune memory (trained immunity) when exposed to certain inflammatory stimuli. Innate immune cells such as monocytes, macrophages, dendritic cells, and natural killer (NK) cells, conditional innate immune cells such as endothelial cells and vascular smooth muscle cells, and non-immune cells were shown to develop trained immunity by undergoing functional reprogramming when exposed to inflammatory stimuli. These stimuli elicit elevated and potentially prolonged/chronic responses to subsequent inflammatory challenges. This long-term reprogramming depends on the rewiring of cell metabolism and epigenetic processes. For example, a few histone modifications have been reported to regulate trained immunity including histone 3 lysine 4 methylation (H3K4me1), H3K4 dimethylation (H3K4me2), H3K4 trimethylation (H3K4me3), H3K9me2, H3K27me3, H3K4 acetylation (H3K4Ac), H3K14Ac, H3K27Ac.Since the field is at the beginning stage, many important questions remain unaddressed. We welcome the submission of Original Research, Systematic Review, Methods. Review, Mini Review, Hypothesis & Theory, Perspective, Clinical Trial, Case Report, Classification, General Commentary, Opinion and Technology & Code focusing on, but not limited to, the following topics:
1. How oxidative stresses regulate trained immunity in pathophysiological conditions
2. How epigenetic modifications such as histone methylations and acetylations regulate trained immunity.
3. How non-coding RNAs regulate trained immunity
The novel insights gained by addressing these questions may lead to identification of new chronic disease risk factors that mediate trained immunity pathways and may potentiate identification of novel therapeutic targets for the treatment of chronic inflammation, and cancers.
