Abstract
SummaryAll organisms are exposed constantly to a variety of infectious and injurious stimuli. These induce inflammatory responses tailored to the threat posed. While the innate immune system is the front line of response to each stimulant, it has been considered traditionally to lack memory, acting in a generic fashion until the adaptive immune arm can take over. This outmoded simplification of the roles of innate and acquired arms of the immune system has been challenged by evidence of myeloid cells altering their response to subsequent encounters based on earlier exposure. This concept of ‘innate immune memory’ has been known for nearly a century, and is accepted among myeloid biologists. In recent years other innate immune cells, such as natural killer cells, have been shown to display memory, suggesting that innate immune memory is a trait common to several cell types. During the last 30 years, evidence has slowly accumulated in favour of not only haematopoietic cells, but also stromal cells, being imbued with memory following inflammatory episodes. A recent publication showing this also to be true in epithelial cells suggests innate immune memory to be widespread, if under‐appreciated, in non‐haematopoietic cells. In this review, we will examine the evidence supporting the existence of innate immune memory in stromal cells. We will also discuss the ramifications of memory in long‐lived tissue‐resident cells. Finally, we will pose questions we feel to be important in the understanding of these forgotten cells in the field of innate memory.
Highlights
In an immune setting, the term ‘memory’ evokes vaccines, memory T cells and the antibody response
Vertebrate–invertebrate divergence preceded the appearance of adaptive immunity, and yet evidence in invertebrates as disparate as meal worm beetles and shrimp, Drosophila and lower metazoans all points towards inflammatory responses altered by prior exposure to infectious agents
Our own work built upon these findings by displaying positive memory to be shared by fibroblast-like synoviocytes (FLS) from both inflamed and non-inflamed joints [37]. While both papers showed gene-specificity of memory in response to endogenous stimuli, the latter displayed trophism, showing that FLS had memory while dermal fibroblasts did not. These findings suggest that inflammatory memory can be a property of the site of origin of fibroblasts rather than disease state
Summary
All organisms are exposed constantly to a variety of infectious and injurious stimuli These induce inflammatory responses tailored to the threat posed. While the innate immune system is the front line of response to each stimulant, it has been considered traditionally to lack memory, acting in a generic fashion until the adaptive immune arm can take over. This outmoded simplification of the roles of innate and acquired arms of the immune system has been challenged by evidence of myeloid cells altering their response to subsequent encounters based on earlier exposure.
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