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Review
. 2021 Oct 22:12:699563.
doi: 10.3389/fimmu.2021.699563. eCollection 2021.

DAMPs and Innate Immune Training

Elisa Jentho  1   2 , Sebastian Weis  2   3
Affiliations
Review

DAMPs and Innate Immune Training

Elisa Jentho et al. Front Immunol. .

Abstract

The ability to remember a previous encounter with pathogens was long thought to be a key feature of the adaptive immune system enabling the host to mount a faster, more specific and more effective immune response upon the reencounter, reducing the severity of infectious diseases. Over the last 15 years, an increasing amount of evidence has accumulated showing that the innate immune system also has features of a memory. In contrast to the memory of adaptive immunity, innate immune memory is mediated by restructuration of the active chromatin landscape and imprinted by persisting adaptations of myelopoiesis. While originally described to occur in response to pathogen-associated molecular patterns, recent data indicate that host-derived damage-associated molecular patterns, i.e. alarmins, can also induce an innate immune memory. Potentially this is mediated by the same pattern recognition receptors and downstream signaling transduction pathways responsible for pathogen-associated innate immune training. Here, we summarize the available experimental data underlying innate immune memory in response to damage-associated molecular patterns. Further, we expound that trained immunity is a general component of innate immunity and outline several open questions for the rising field of pathogen-independent trained immunity.

Keywords: DAMP; heme; oxLDL; trained innate immunity; vimentin.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

Figure 1
Figure 1
Classical in vitro model of trained immunity. Trained immunity describes a functional, metabolic and epigenetic adaptation of innate immune cells to previous stimuli with ensuing increased immune response, i.e. cytokine release, to secondary stimulation. (A) The classical model applies the Dectin-1 agonist β-1,3-D Glucan as the first stimulus and the TLR-4 agonist LPS as the second stimulus. (B) The basis for β-1,3-D Glucan induced trained immunity are metabolic adaptations, including the mTOR signal-transduction enhanced glycolysis. Interrupted errors indicate that many more proteins are involved in the signaling cascade, which are not depicted in the figure.
See this image and copyright information in PMC

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