c-Kit-positive ILC2s exhibit an ILC3-like signature that may contribute to IL-17-mediated pathologies

Bernink, Jochem H.; Ohne, Yoichiro; Teunissen, Marcel B. M.; Wang, Jingya; Wu, Jincheng; Krabbendam, Lisette; Guntermann, Christine; Volckmann, Richard; Koster, Jan; Tol, Sophie van; Ramírez, Iván Hernández; Shrestha, Yashaswi; Rie, Menno A. de; Spits, Hergen; Ros, Xavier Romero; Humbles, Alison A.

doi:10.1038/s41590-019-0423-0

Cited by 151 publications

(188 citation statements)

References 47 publications

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“…46 A subpopulation of ILC2s that can convert into IL-17-producing NKp44-ILC3-like cells has recently been identified. 38 However, in our study lung…”

Section: Discussioncontrasting

confidence: 57%

IL‐1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early‐life rhinovirus infection in mice

Han

Ishikawa

Bermick

et al. 2020

Allergy

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Background: Early-life wheezing-associated respiratory infection with human rhinovirus (RV) is associated with asthma development. RV infection of 6-day-old immature mice causes mucous metaplasia and airway hyperresponsiveness which is associated with the expansion of IL-13-producing type 2 innate lymphoid cells (ILC2s) and dependent on IL-25 and IL-33. We examined regulation of this asthma-like phenotype by IL-1β.

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“…46 A subpopulation of ILC2s that can convert into IL-17-producing NKp44-ILC3-like cells has recently been identified. 38 However, in our study lung…”

Section: Discussioncontrasting

confidence: 57%

IL‐1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early‐life rhinovirus infection in mice

Han

Ishikawa

Bermick

et al. 2020

Allergy

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“…Furthermore, ILC2s can be divided into conventional ILC2s and inflammatory ILC2s induced by IL-33 and IL-25, respectively. 82,83 Recent studies have also found IL-10-producing ILC2s, 84 and IL-17-producing ILC2s 41,85 in allergic airway inflammation. However, whether myeloid cells can affect ILC2 plasticity in health and disease remains to be investigated.…”

Section: Discussionmentioning

confidence: 96%

Role of myeloid cells in the regulation of group 2 innate lymphoid cell‐mediated allergic inflammation

Lei

Yang

et al. 2020

Immunology

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“…Differently, an increased tumor growth was described in IL-9R deficient mouse; ILC2s together with Th9-cells are an important source of IL-9 in inflammatory conditions and TGF-β is able to induce IL-9 production by ILC2s, thus we cannot exclude that in the tumor microenvironment TGF-β-induced IL-9 release by ILC2s may elicit anti-tumor activity of these cells [89][90][91]. Recently, a crucial role for TGF-β in driving the trans-differentiation of ILC2s into ILC3s has been shown in inflammatory conditions [92]. In this context, TGF-β induced-IL-23R expression on a distinct subset of ILC2s expressing the c-kit receptor allowed these cells to respond to IL-23 and to produce the pro-inflammatory cytokine IL-17.…”

Section: Guide Of Ilc Plasticity By Tgf-β In Cancermentioning

confidence: 95%

Hitting More Birds with a Stone: Impact of TGF-β on ILC Activity in Cancer

Fionda

Stabile

Cerboni

et al. 2020

JCM

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Transforming growth factor (TGF)-β is a central immunosuppressive cytokine within tumor microenvironment inhibiting the expansion and function of major cellular components of adaptive and innate immune system. Among them, compelling evidence has demonstrated that TGF-β is a key regulator of natural killer (NK) cells, innate lymphoid cells (ILCs) with a critical role in immunosurveillance against different kinds of cancer cells. A TGF-β rich tumor microenvironment blocks NK cell activity at multiple levels. This immunosuppressive factor exerts direct regulatory effects on NK cells including inhibition of cytokine production, alteration of activating/inhibitory receptor expression, and promotion of the conversion into non cytotoxic group I ILC (ILC1). Concomitantly, TGF-β can render tumor cells less susceptible to NK cell-mediated recognition and lysis. Indeed, accumulating evidence suggest that changes in levels of NKG2D ligands, mainly MICA, as well as an increase of immune checkpoint inhibitors (e.g., PD-L1) and other inhibitory ligands on cancer cells significantly contribute to TGF-β-mediated suppression of NK cell activity. Here, we will take into consideration two major mechanisms underlying the negative regulation of ILC function by TGF-β in cancer. First, we will address how TGF-β impacts the balance of signals governing NK cell activity. Second, we will review recent advances on the role of this cytokine in driving ILC plasticity in cancer. Finally, we will discuss how the development of therapeutic approaches blocking TGF-β may reverse the suppression of host immune surveillance and improve anti-tumor NK cell response in the clinic.

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c-Kit-positive ILC2s exhibit an ILC3-like signature that may contribute to IL-17-mediated pathologies

Cited by 151 publications

References 47 publications

IL‐1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early‐life rhinovirus infection in mice

IL‐1β prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early‐life rhinovirus infection in mice

Role of myeloid cells in the regulation of group 2 innate lymphoid cell‐mediated allergic inflammation

Hitting More Birds with a Stone: Impact of TGF-β on ILC Activity in Cancer

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