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Signal-Strength and History-Dependent Innate Immune Memory Dynamics in Health and Disease

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Toll-like Receptors in Health and Disease

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 276))

Abstract

Innate immunity exhibits memory characteristics, reflected not only in selective recognition of external microbial or internal damage signals, but more importantly in history and signal-strength dependent reprogramming of innate leukocytes characterized by priming, tolerance, and exhaustion. Key innate immune cells such as monocytes and neutrophils can finely discern and attune to the duration and intensity of external signals through rewiring of internal signaling circuitries, giving rise to a vast array of discreet memory phenotypes critically relevant to managing tissue homeostasis as well as diverse repertoires of inflammatory conditions. This review will highlight recent advances in this rapidly expanding field of innate immune programming and memory, as well as its translational implication in the pathophysiology of selected inflammatory diseases.

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Abbreviations

ABCA1:

ATP-binding cassette sub-family A member 1

ABCG1:

ATP-binding cassette sub-family G member 1

ACE:

Angiotensin-converting enzyme

APC:

Antigen presenting cells

ApOE:

Apolipoprotein E

ATG:

Autophagy-related gene

BCG:

Bacillus Calmette-Guérin

BCR:

B cell receptor

CCL:

C-C motif chemokine ligand

CCR:

C-C Chemokine receptor

CLP:

Cecal ligation and puncture

CMP:

Common myeloid progenitor

CTLA-4:

Cytotoxic T-lymphocyte-associated protein 4

CXCL:

C-X-C motif chemokine ligand

CXCR:

C-X-C motif chemokine receptors

DAMP:

Damage-associated molecular pattern

ERK1/2:

Extracellular signal-regulated kinase 1/2

G-CSF:

Granulocyte-colony stimulating factor

GM-CSF:

Granulocyte-macrophage colony stimulating factor

GMP:

Granulocyte-monocyte progenitors

GPNMB :

Glycoprotein-Nmb

GRK2:

G protein-coupled receptor kinases

HGF:

Hepatocyte growth factor

HSC:

Hematopoietic stem cell

ICAM1:

Intercellular adhesion molecule 1

IL:

Interleukin

iNOS:

Inducible nitric oxide synthase

IRAK-M:

Interleukin-1R-associated-kinase- M

JMJD3:

Jumonji domain containing 3

KDM6B:

Lysine demethylase 6B

LAG-3:

Lymphocyte-activating gene

Ldlr:

Low-density lipoprotein receptor

LPS:

Lipopolysaccharide

LTB4:

Leukotriene B4

MAL:

MyD88-adapter-like

MCP:

Monocyte chemoattractant protein

M-CSF:

Macrophage-colony-stimulating factor

MEP:

Megakaryocyte-erythrocyte progenitor

MMP:

Matrix metalloproteinases

MYD88:

Myeloid differentiation factor 88

NET:

Neutrophil extracellular trap

NOX2:

NADPH oxidase 2

oxLDL:

Oxidized low-density lipoprotein

PAMP:

Pathogen associated molecular pattern

PD-1:

Programmed cell death protein-1

PD-L1:

Programmed death-ligand 1

PI3K/AKT:

Phosphatidylinositol-3-kinase and protein kinase B

SFK:

Src family kinases

SR-A:

Scavenger receptor class A

SR-B1:

Scavenger receptor class B type 1

STAT:

Signal transducer and activator of transcription

TAM:

Tumor-associated macrophages

TAN:

Tumor-associated neutrophils

TCR:

T cell receptor

TIM-3:

T-cell immunoglobulin and mucin-domain containing-3

TLR:

Toll-like receptor

TNF:

Tumor necrosis factor

TRAM:

Toll/IL-1R domain-containing adaptor-inducing IFN-β-related adaptor molecule

TRIF:

Toll/IL-1R domain-containing adaptor-inducing IFN-β

VEGF:

Vascular endothelial growth factor

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Authors and Affiliations

  1. Department of Biological Sciences, Virginia Tech, Blacksburg, VA, USA

    Shuo Geng, Kisha Pradhan & Liwu Li

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  1. Shuo Geng
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  2. Kisha Pradhan
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  3. Liwu Li
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Correspondence to Liwu Li .

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Editors and Affiliations

  1. Department of Pediatrics, Division of Allergy and Immunology, Duke University Medical Center (DUMC), Durham, NC, USA

    Vijay Kumar

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Geng, S., Pradhan, K., Li, L. (2021). Signal-Strength and History-Dependent Innate Immune Memory Dynamics in Health and Disease. In: Kumar, V. (eds) Toll-like Receptors in Health and Disease. Handbook of Experimental Pharmacology, vol 276. Springer, Cham. https://doi.org/10.1007/164_2021_485

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