Human TH17 cell development requires processing of dendritic cell–derived CXCL8 by neutrophil elastase

Souwer, Yuri; Kormelink, Tom Groot; Taanman-Kueter, Esther W. M.; Muller, Femke J. M.; Capel, Toni M.M. van; Varga, Domonkos V.; Bar-Ephraïm, Yotam E.; Teunissen, Marcel B. M.; Ham, S. Marieke van; Kuijpers, Taco W.; Wouters, Diana; Meyaard, Linde; Jong, Esther C. de

doi:10.1016/j.jaci.2018.01.003

Cited by 39 publications

(70 citation statements)

References 16 publications

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“…Moreover, GM‐CSF and/or IFN‐γ derived from Th17 cells were shown to promote neutrophil survival as well as enhance various neutrophil effector functions . More recently, neutrophil‐derived elastase has been shown to process dendritic cell‐derived CXCL8 into a truncated, potent Th17 cell‐inducing form . Our current data on the ability of TLR8‐activated neutrophils to also drive via IL‐23 the differentiation of Th17 cells, is consistent with another study showing that Group B Streptococcus (GBS)‐stimulated neonatal neutrophils induce robust Th1‐ and Th17‐type responses in neonatal CD4 + T cell and Treg populations through mechanisms involving cell‐cell contact and soluble mediators, adding new knowledge on the regulation and activation of the neutrophil/Th17 cell crosstalk.…”

Section: Discussionsupporting

confidence: 89%

“…48 More recently, neutrophil-derived elastase has been shown to process dendritic cell-derived CXCL8 into a truncated, potent Th17 cell-inducing form. 49 Our data greatly extend previous observations on the ability of human neutrophils to express/produce IL-23. For example, it was previously shown that, while Helicobacter pylori Neutrophil Activating Factor triggers the expression of IL-23p19 mRNA by human neutrophils, 51…”

Section: Discussionsupporting

confidence: 86%

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Human neutrophils activated via TLR8 promote Th17 polarization through IL-23

Tamassia

Arruda‐Silva

Wright

et al. 2019

Journal of Leukocyte Biology

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Human neutrophils contribute to the regulation of inflammation via the generation of a range of cytokines that affect all elements of the immune system. Here, we investigated their ability to express some of the members of the IL‐12 family after incubation with TLR8 agonists. Highly pure human neutrophils were thus incubated for up to 48 h with or without R848, or other TLR8 agonists, to then measure the expression levels of transcripts and proteins for IL‐12 family member subunits by RNA‐seq, reverse transcription quantitative PCR, and ELISA. We show a TLR8‐mediated inducible expression of IL‐12B and IL‐23A, but not IL‐12A, mRNA, which occurs via chromatin remodeling (as assessed by ChIP‐seq), and subsequent production of IL‐23 and IL‐12B, but no IL‐12, proteins. Induction of IL‐23 requires endogenous TNF‐α, as both mRNA and protein levels were blocked in TLR8‐activated neutrophils via a TNF‐α‐neutralizing Ab. We also show that supernatants from TLR8‐activated neutrophils, but not autologous monocytes, induce the differentiation of Th17 cells from naïve T cells in an IL‐23‐dependent fashion. This study unequivocally demonstrates that highly pure human neutrophils express and produce IL‐23, further supporting the key roles played by these cells in the important IL‐17/IL‐23 network and Th17 responses.

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Section: Discussionsupporting

confidence: 89%

Section: Discussionsupporting

confidence: 86%

Human neutrophils activated via TLR8 promote Th17 polarization through IL-23

Tamassia

Arruda‐Silva

Wright

et al. 2019

Journal of Leukocyte Biology

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“…1 The importance of neutrophils in the HS pathogenesis is underlined by the increased levels of CXCL-8 that can be cleaved by neutrophil elastase to activate Th17 cells to produce bioactive IL-17. 7 Some previously published results, that showed significant upregulation of TNF-α, IL-1ß, and IL-10 in (peri)lesional HS skin, could not be confirmed statistically. 8,9 This can be explained by the different approaches as in our study biopsies were homogenized for in situ assessment, while van der Zee et al and Kelly et al cultured the skin biopsies for, respectively, 24 and 3 hours.…”

mentioning

confidence: 84%

Novel cytokine and chemokine markers of hidradenitis suppurativa reflect chronic inflammation and itch

Vossen

Zee

Tsoi

et al. 2018

Allergy

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“…Neutrophils are now known to be involved in orchestrating adaptive immune responses by influencing various cell types, either by releasing multiple soluble mediators or via direct cellular contacts. For instance, neutrophils can modulate DC migration, maturation, and their CD4 + T cell polarizing capacity [ 2 , 80 ]. In addition, they can suppress or enhance B cell, CD4 + T cell, and γδ T cell functions (independent of MHC), or even act as antigen-presenting cells under specific activating conditions and thereby drive antigen-specific T cell responses [ 10 , 79 ].…”

Section: Neutrophilsmentioning

confidence: 99%

The role of extracellular vesicles when innate meets adaptive

et al. 2018

Self Cite

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Innate immune cells are recognized for their rapid and critical contribution to the body’s first line of defense against invading pathogens and harmful agents. These actions can be further amplified by specific adaptive immune responses adapted to the activating stimulus. Recently, the awareness has grown that virtually all innate immune cells, i.e., mast cells, neutrophils, macrophages, eosinophils, basophils, and NK cells, are able to communicate with dendritic cells (DCs) and/or T and B cells, and thereby significantly contribute to the orchestration of adaptive immune responses. The means of communication that are thus far primarily associated with this function are cell-cell contacts and the release of a broad range of soluble mediators. Moreover, the possible contribution of innate immune cell-derived extracellular vesicles (EVs) to the modulation of adaptive immunity will be outlined in this review. EVs are submicron particles composed of a lipid bilayer, proteins, and nucleic acids released by cells in a regulated fashion. EVs are involved in intercellular communication between multiple cell types, including those of the immune system. A good understanding of the mechanisms by which innate immune cell-derived EVs influence adaptive immune responses, or vice versa, may reveal novel insights in the regulation of the immune system and can open up new possibilities for EVs (or their components) in controlling immune responses, either as a therapy, target, or as an adjuvant in future immune modulating treatments.

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Human TH17 cell development requires processing of dendritic cell–derived CXCL8 by neutrophil elastase

Abstract: Polymorphisms related to ORMDL3 are associated with asthma susceptibility, alterations in transcriptional regulation of ORMDL3, and changes in TH2 cytokine levels.

Cited by 39 publications

References 16 publications

Human neutrophils activated via TLR8 promote Th17 polarization through IL-23

Human neutrophils activated via TLR8 promote Th17 polarization through IL-23

Novel cytokine and chemokine markers of hidradenitis suppurativa reflect chronic inflammation and itch

The role of extracellular vesicles when innate meets adaptive

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