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Putting the brakes on ILC2 cells

Nature Immunology volume 17, pages 43–44 (2016)Cite this article

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Immune responses are characterized by the concerted actions of both effector mechanisms and regulatory mechanisms. Signaling via the transcription factor STAT1 downstream of receptors for interferons and interleukin 27 (IL-27) can suppress type 2 immune responses induced by group 2 innate lymphoid cells (ILCs).

Innate lymphoid cells (ILCs) reside in the skin, lung and intestine, participate in local immune responses and fulfill essential homeostatic functions at these sites. Three subsets of ILCs (ILC1, ILC2 and ILC3) have been documented that mirror the CD4+ helper T cell subsets (TH1, TH2 or TH17) in their transcription factor expression and resulting effector functions. ILC2 cells express the zinc-finger transcription factor GATA-3, produce the type 2 cytokines interleukin 5 (IL-5) and IL-13, and serve an important role in the defense against helminth infection and the induction of airway hyper-reactivity after exposure to allergens or viral respiratory infection1. A role for ILC2 cells in visceral adipose tissues in regulating metabolic homeostasis has also been reported, which shows that loss of ILC2 cells is associated with the development of insulin resistance in obese mice2. Thus, understanding how ILC2 responses are regulated would reveal new therapeutic approaches for the treatment of a wide range of severe diseases. Type 1 and type 2 immunity tightly counter-regulate each other. Early reports demonstrated a role for interferons and the TH1 lineage–specifying T-box transcription factor T-bet (encoded by Tbx21) in suppressing the infiltration of eosinophils into the lungs and airway hyper-reactivity. This phenomenon has been partially associated with the ability of these factors to promote TH1 differentiation and suppress TH2 differentiation3,4, although tissue effects downstream of the secretion of TH2 cytokines can be observed5. Reports by Duerr et al.6 and Moro et al.7 in this issue of Nature Immunology demonstrate that sensing of interferons is also a mechanism that regulates ILC2-mediated responses and identify STAT1, a central signal-transduction molecule downstream of the receptors for interferons and IL-27, as the main executor of such functions.

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Figure 1: STAT1 regulates ILC2 cells.

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Authors and Affiliations

  1. Christina Stehle and Chiara Romagnani are in the Department of Innate Immunity, Deutsches Rheuma Forschungszentrum Berlin, Leibniz-Gemeinschaft, Berlin, Germany.,

    Christina Stehle & Chiara Romagnani

  2. Philippe Saikali is in the Department of Experimental Immunology, Deutsches Rheuma Forschungszentrum Berlin, Leibniz-Gemeinschaft, Berlin, Germany.,

    Philippe Saikali

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  1. Christina Stehle
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Correspondence to Chiara Romagnani.

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Stehle, C., Saikali, P. & Romagnani, C. Putting the brakes on ILC2 cells. Nat Immunol 17, 43–44 (2016). https://doi.org/10.1038/ni.3353

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