Abstract
ABSTRACTTrained immunity was originally proposed as a program of innate immunity memory by innate immunity cells of hematopoietic origin such as the monocytes/macrophages and the NK cells. Here I discuss some old and new data justifying this program and some specific, still unanswered, questions it raises regarding the model fungus Candida albicans and the chronic, inflammatory vulvovaginal disease it causes. Building upon this well-established program, the recent reports that epithelial cells of mammals can also acquire memory from previous stimulations, and the apparent intrinsic ability of many living cells from bacteria to mammals to learn from experience, I suggest an expansion of the concept of trained immunity to include all cells of different lineages with the potential of memorizing previous microbial encounters. This expansion would better fit the complexity of innate immunity and the role it plays in infectious and inflammatory diseases.
Highlights
Trained immunity was originally proposed as a program of innate immunity memory by innate immunity cells of hematopoietic origin such as the monocytes/macrophages and the NK cells
While the existence of an “adaptive” or “memory” component of innate immunity was suspected or suggested [1, 2], Netea and collaborators first proposed the term trained immunity to conceptualize all evidence for an anti-infectious, protective, memory response entirely mediated by cells of innate immunity [3,4,5]
Common to all organisms appears to be the molecular basis of the phenomenon which relies upon specific epigenetic reprogramming of innate immune cells, with chromatin remodeling, changes in gene transcription, and a profound metabolic shift [9, 10]
Summary
Trained immunity was originally proposed as a program of innate immunity memory by innate immunity cells of hematopoietic origin such as the monocytes/macrophages and the NK cells. Trained immunity (TI) is a persistent (weeks to months) immunomodulation of cells of innate immunity of hematopoietic lineage, monocytes/macrophages, due to memory acquisition upon microbial or nonmicrobial stimulation.
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