Activated plasmacytoid dendritic cells regulate type 2 innate lymphoid cell–mediated airway hyperreactivity

Maazi, Hadi; Banie, Homayon; Muench, German R. Aleman; Patel, Nisheel; Wang, Bowen; Sankaranarayanan, Ishwarya; Bhargava, Vipul; Sato, Takahiro; Lewis, Gavin; Cesaroni, Matteo; Karras, James G.; Das, Anuk; Soroosh, Pejman; Akbari, Omid

doi:10.1016/j.jaci.2017.04.043

Cited by 62 publications

(63 citation statements)

References 49 publications

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“…Many different groups have confirmed that type 1 IFNs, type 2 IFN, and IL‐27 suppress the proliferation and type 2 cytokine production from mouse and human ILC2s . Specifically, IFN‐β and IFN‐γ strongly suppress the activation of mouse ILC2s in response to IL‐33 or IL‐2 + IL‐25 stimulation .…”

Section: Suppressive Cytokines (Type 1 Ifns Type 2 Ifn (Ifn‐γ) Il‐2mentioning

confidence: 97%

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The group 2 innate lymphoid cell (ILC2) regulatory network and its underlying mechanisms

Kabata

Moro

Koyasu

2018

Immunological Reviews

217

183

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Summary Group 2 innate lymphoid cells (ILC2s) play critical roles in the induction of type 2 inflammation, response to parasite infection, metabolic homeostasis, and tissue repair. These multifunctional roles of ILC2s are tightly controlled by complex regulatory systems in the local microenvironment, the disruption of which may cause various health problems. This review summarizes up‐to‐date knowledge regarding positive and negative regulators for ILC2s based on their function and signaling pathways, including activating cytokines (IL‐33, IL‐25; MAPK, NF‐κB pathways), co‐stimulatory cytokines (IL‐2, IL‐7, IL‐9, TSLP; STAT5, IL‐4; STAT6, TNF superfamily; MAPK, NF‐κB pathways), suppressive cytokines (type1 IFNs, IFN‐γ, IL‐27; STAT1, IL‐10, TGF‐β), transdifferentiation cytokines (IL‐12; STAT4, IL‐1β, IL‐18), lipid mediators (LTC4, LTD4, LTE4, PGD2; Ca2+‐NFAT pathways, PGE2, PGI2; AC/cAMP/PKA pathways, LXA4, LTB4), neuropeptides (NMU; Ca2+‐NFAT, MAPK pathways, VIP, CGRP, catecholamine, acetylcholine), sex hormones (androgen, estrogen), nutrients (butyrate; HDAC inhibitors, vitamins), and cell‐to‐cell interactions (ICOSL‐ICOS; STAT5, B7‐H6‐NKp30, E‐cadherin‐KLRG1). This comprehensive review affords a better understanding of the regulatory network system for ILC2s, providing impetus to develop new treatment strategies for ILC2‐related health problems.

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Section: Suppressive Cytokines (Type 1 Ifns Type 2 Ifn (Ifn‐γ) Il‐2mentioning

confidence: 97%

“…IFNs are produced by NK cells, NKT cells, dendritic cells, and T cells during inflammation . In influenza virus infection, type 1 interferon receptor‐deficient mice exhibit more severe ILC2‐mediated eosinophil inflammation .…”

Section: Suppressive Cytokines (Type 1 Ifns Type 2 Ifn (Ifn‐γ) Il‐2mentioning

confidence: 99%

The group 2 innate lymphoid cell (ILC2) regulatory network and its underlying mechanisms

Kabata

Moro

Koyasu

2018

Immunological Reviews

217

183

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“…Therefore, negative regulation of ILC2s is crucial to prevent pathologic type 2 inflammation. Cytokines associated with type 1 immunity, such as type I interferons (IFNs) [48], IFN-γ [49–52] and IL-27 [50] are dominant inhibitors of ILC2 activation. Androgen receptor (AR) signaling on ILC2s restricts their activation, and may account for the lower susceptibility to allergic airway inflammation in males [53,54].…”

Section: Regulation Of Ilc2 Activation In Barrier Tissuesmentioning

confidence: 99%

All along the watchtower: group 2 innate lymphoid cells in allergic responses

Dahlgren

Molofsky

2018

Current Opinion in Immunology

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Group 2 innate lymphoid cells (ILC2) are a subset of innate lymphocytes that responds to local, tissue-derived signals and initiates allergic immune responses. ILC2 activation promotes the recruitment of eosinophils, polarization of alternatively activated macrophages, and tissue-remodeling, processes associated with the 'weep and sweep' response to helminthic worm colonization and infection. ILC2s also coordinate both physiologic and pathologic type 2 allergic immune responses, including promoting normal tissue development and remodeling and driving allergic pathology such as atopic dermatitis and allergic asthma. In this review we summarize recent advances in ILC2 biology, particularly focusing on how local cells and signals coordinately regulate ILC2s, how this may influence physiologic processes, and how ILC2 cooperate with adaptive T helper type 2 cells to drive pathologic allergic inflammation.

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“…In contrast to ILC2‐activating epithelial‐ or endothelial‐derived cytokines, other cytokines, including type I and type II IFNs (3–6), IL‐27 (3, 4, 7) and the TNF family cytokine TL1A (8, 9), that are produced by the innate and adaptive immune systems can suppress ILC2 responses. In addition to cytokines, cell‐surface molecules, such as inducible T‐cell costimulator (ICOS) (5, 10) and programmed death‐1 (11), eicosanoids, including leukotrienes (12) and prostaglandin D 2 (13), and hormones, including androgens (14) and corticosteroids (15), have all been shown to regulate ILC2s.…”

mentioning

confidence: 99%

“…Among ILCs, group 2 ILCs (ILC2s) respond to epithelial or endothelial cell-derived cytokines, such as IL-25, IL-33, and thymic stromal lymphopoietin (TSLP), by proliferating and producing copious amounts of type 2 cytokines, such as IL-5, IL-6, IL-9, IL-13, and amphiregulin, which mediate the effector pathways that are vital for antihelminth immune responses and the development of allergic inflammation (2). In contrast to ILC2-activating epithelial-or endothelial-derived cytokines, other cytokines, including type I and type II IFNs (3)(4)(5)(6), IL-27 (3,4,7) and the TNF family cytokine TL1A (8,9), that are produced by the innate and adaptive immune systems can suppress ILC2 responses. In addition to cytokines, cell-surface molecules, such as inducible T-cell costimulator (ICOS) (5,10) and programmed death-1 (11), eicosanoids, including leukotrienes (12) and prostaglandin D 2 (13), and hormones, including androgens (14) and corticosteroids (15), have all been shown to regulate ILC2s.…”

mentioning

confidence: 99%

Adenosine receptors differentially regulate type 2 cytokine production by IL‐33–activated bone marrow cells, ILC2s, and macrophages

Csóka

Németh

Duerr³

et al. 2018

FASEB j.

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Group 2 innate lymphoid cells (ILC2s) represent a rapid source of type 2 cytokines, such as IL-5 and IL-13, and play an important role in orchestrating type 2 immune response. Adenosine is an endogenous purine nucleoside, a catabolite of ATP that binds and activates ≥1 of 4 transmembrane G protein-coupled cell-surface adenosine receptors (ARs)-A, A, A, and A. Here, we studied the role of ARs in the regulation of cytokine production by ILC2s. We found that AARs suppress the production of both IL-5 and IL-13 by ILC2s, whereas AARs augment IL-5 production and fail to affect IL-13 release. Combined stimulation of all ARs led to the suppression of both IL-5 and IL-13 production, which indicated that AARs dominate AARs. Both pre- and post-transcriptional processes may be involved in the AR modulation of ILC2 IL-5 and IL-13 production. Thus, we identify adenosine as a novel negative regulator of ILC2 activation.-Csóka, B., Németh, Z. H., Duerr, C. U., Fritz, J. H., Pacher, P., Haskó, G. Adenosine receptors differentially regulate type 2 cytokine production by IL-33-activated bone marrow cells, ILC2s, and macrophages.

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Activated plasmacytoid dendritic cells regulate type 2 innate lymphoid cell–mediated airway hyperreactivity

Cited by 62 publications

References 49 publications

The group 2 innate lymphoid cell (ILC2) regulatory network and its underlying mechanisms

The group 2 innate lymphoid cell (ILC2) regulatory network and its underlying mechanisms

All along the watchtower: group 2 innate lymphoid cells in allergic responses

Adenosine receptors differentially regulate type 2 cytokine production by IL‐33–activated bone marrow cells, ILC2s, and macrophages

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