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Review
. 2016 Sep;68(9):2071-82.
doi: 10.1002/art.39745. Epub 2016 Jul 29.

Review: Neutrophils as Invigorated Targets in Rheumatic Diseases

Peter C Grayson  1 , Christine Schauer  2 , Martin Herrmann  2 , Mariana J Kaplan  1
Affiliations
Review

Review: Neutrophils as Invigorated Targets in Rheumatic Diseases

Peter C Grayson et al. Arthritis Rheumatol. 2016 Sep.
No abstract available

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Figures

Figure 1
Figure 1. Characteristics of neutrophils
Neutrophils are multifunctional granulocytes that contribute to pathology across a spectrum of inflammatory diseases. Activation of neutrophils can occur through a variety of specific receptors including pattern recognition receptors and Fc receptors. Activation of the inflammasome by pathogens or danger signals, such as intracellular monosodium urate crystals, can lead to production of inflammatory cytokines including IL-1β. Secretion of cytokines/chemokines and antigen presentation by MHC Class II receptors can coordinate broader immune responses. Peptidylarginine deiminase enzymes contribute to the formation of neutrophil extracellular traps (NETs). NETs serve a variety of immunogenic and immunosuppressive functions in human disease, including externalization of modified antigens. Reactive oxygen species (ROS) are produced intracellularly through multiple mechanisms including the NADPH complex and mitochondria. Degranulation of the antimicrobial, cytoxic contents within various types of neutrophil granules can be toxic to the local tissue environment. Key regulators of neutrophil function may constitute novel therapeutic targets. Abbreviations: NF-KB= nuclear factor kappa-light-chain-enhancer of activated B cells; ASC = apoptosis-associated speck-like protein containing CARD; NLRP3 also known as cryopyrin or NALP3; MPO = myeloperoxidase; H202 = hydrogen peroxide.
Figure 2
Figure 2. Neutrophil extracellular traps
Human control neutrophils were induced to undergo NET formation with LPS stimulation. Red represents MPO and blue represents DNA. Magnification is 40X. Photograph obtained by Dr. Carolyne Smith, Systemic Autoimmunity Branch, NIAMS/NIH.
Figure 3
Figure 3. NETs in gouty arthritis
In areas of low neutrophil densities, individual netting neutrophils trap MSU-crystals in an inflammatory manner, releasing their load of pro-inflammatory mediators (acute inflammation). After the release of chemokines (e.g. IL-8) further neutrophils are attracted and the density of neutrophils rises. The NETting neutrophils clump together and form aggregates (aggNETs). These structures initially trap and finally degrade the inflammatory mediators and thus initiate the resolution of inflammation.
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