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      ILC3 function as a double-edged sword in inflammatory bowel diseases

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          Abstract

          Inflammatory bowel diseases (IBD), composed mainly of Crohn’s disease (CD) and ulcerative colitis (UC), are strongly implicated in the development of intestinal inflammation lesions. Its exact etiology and pathogenesis are still undetermined. Recently accumulating evidence supports that group 3 innate lymphoid cells (ILC3) are responsible for gastrointestinal mucosal homeostasis through moderate generation of IL-22, IL-17, and GM-CSF in the physiological state. ILC3 contribute to the progression and aggravation of IBD while both IL-22 and IL-17, along with IFN-γ, are overexpressed by the dysregulation of NCR − ILC3 or NCR + ILC3 function and the bias of NCR + ILC3 towards ILC1 as well as regulatory ILC dysfunction in the pathological state. Herein, we feature the group 3 innate lymphoid cells’ development, biological function, maintenance of gut homeostasis, mediation of IBD occurrence, and potential application to IBD therapy.

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          Group 2 innate lymphoid cells promote beiging of white adipose tissue and limit obesity.

          Jonathan R. Brestoff, Brian S Kim, Steven A Saenz … (2015)
          Obesity is an increasingly prevalent disease regulated by genetic and environmental factors. Emerging studies indicate that immune cells, including monocytes, granulocytes and lymphocytes, regulate metabolic homeostasis and are dysregulated in obesity. Group 2 innate lymphoid cells (ILC2s) can regulate adaptive immunity and eosinophil and alternatively activated macrophage responses, and were recently identified in murine white adipose tissue (WAT) where they may act to limit the development of obesity. However, ILC2s have not been identified in human adipose tissue, and the mechanisms by which ILC2s regulate metabolic homeostasis remain unknown. Here we identify ILC2s in human WAT and demonstrate that decreased ILC2 responses in WAT are a conserved characteristic of obesity in humans and mice. Interleukin (IL)-33 was found to be critical for the maintenance of ILC2s in WAT and in limiting adiposity in mice by increasing caloric expenditure. This was associated with recruitment of uncoupling protein 1 (UCP1)(+) beige adipocytes in WAT, a process known as beiging or browning that regulates caloric expenditure. IL-33-induced beiging was dependent on ILC2s, and IL-33 treatment or transfer of IL-33-elicited ILC2s was sufficient to drive beiging independently of the adaptive immune system, eosinophils or IL-4 receptor signalling. We found that ILC2s produce methionine-enkephalin peptides that can act directly on adipocytes to upregulate Ucp1 expression in vitro and that promote beiging in vivo. Collectively, these studies indicate that, in addition to responding to infection or tissue damage, ILC2s can regulate adipose function and metabolic homeostasis in part via production of enkephalin peptides that elicit beiging.
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            Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus

            Laurel A. Monticelli, Gregory Sonnenberg, Michael C. Abt … (2011)
            Article 0 comments Cited 382 times – based on 0 reviews     Review now
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              Ustekinumab induction and maintenance therapy in refractory Crohn's disease.

              William J Sandborn, Christopher R Gasink, Long-Long Gao … (2012)
              In patients with Crohn's disease, the efficacy of ustekinumab, a human monoclonal antibody against interleukin-12 and interleukin-23, is unknown. We evaluated ustekinumab in adults with moderate-to-severe Crohn's disease that was resistant to anti-tumor necrosis factor (TNF) treatment. During induction, 526 patients were randomly assigned to receive intravenous ustekinumab (at a dose of 1, 3, or 6 mg per kilogram of body weight) or placebo at week 0. During the maintenance phase, 145 patients who had a response to ustekinumab at 6 weeks underwent a second randomization to receive subcutaneous injections of ustekinumab (90 mg) or placebo at weeks 8 and 16. The primary end point was a clinical response at 6 weeks. The proportions of patients who reached the primary end point were 36.6%, 34.1%, and 39.7% for 1, 3, and 6 mg of ustekinumab per kilogram, respectively, as compared with 23.5% for placebo (P=0.005 for the comparison with the 6-mg group). The rate of clinical remission with the 6-mg dose did not differ significantly from the rate with placebo at 6 weeks. Maintenance therapy with ustekinumab, as compared with placebo, resulted in significantly increased rates of clinical remission (41.7% vs. 27.4%, P=0.03) and response (69.4% vs. 42.5%, P<0.001) at 22 weeks. Serious infections occurred in 7 patients (6 receiving ustekinumab) during induction and 11 patients (4 receiving ustekinumab) during maintenance. Basal-cell carcinoma developed in 1 patient receiving ustekinumab. Patients with moderate-to-severe Crohn's disease that was resistant to TNF antagonists had an increased rate of response to induction with ustekinumab, as compared with placebo. Patients with an initial response to ustekinumab had significantly increased rates of response and remission with ustekinumab as maintenance therapy. (Funded by Janssen Research and Development; CERTIFI ClinicalTrials.gov number, NCT00771667.).
              Article 0 comments Cited 352 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Changjiang Dong: 0044-1334-769074 , c.dong@uea.ac.uk
                Jing Liu: 0086-20-85227010 , tjliu@jnu.edu.cn
                Feiyue Xing: 0086-20-85220723 , tfyxing@jnu.edu.cn
                Journal
                Journal ID (nlm-ta): Cell Death Dis
                Journal ID (iso-abbrev): Cell Death Dis
                Title: Cell Death & Disease
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2041-4889
                Publication date (Electronic): 8 April 2019
                Publication date PMC-release: 8 April 2019
                Publication date Collection: April 2019
                Volume: 10
                Issue: 4
                Electronic Location Identifier: 315
                Affiliations
                [1 ]ISNI 0000 0004 1790 3548, GRID grid.258164.c, Institute of Tissue Transplantation and Immunology, Department of Immunobiology, , Jinan University, ; Guangzhou, China
                [2 ]ISNI 0000 0004 1790 3548, GRID grid.258164.c, Key Laboratory of Functional Protein Research of Guangdong, Higher Education Institutes, , Jinan University, ; Guangzhou, China
                [3 ]ISNI 0000 0004 1790 3548, GRID grid.258164.c, School of Stomatology, , Jinan University, ; Guangzhou, China
                [4 ]ISNI 0000 0001 1092 7967, GRID grid.8273.e, BioMedical Research Centre, , University of East Anglia, ; NR4 7TJ Norwich, UK
                Article
                Publisher ID: 1540
                DOI: 10.1038/s41419-019-1540-2
                PMC ID: 6453898
                PubMed ID: 30962426
                SO-VID: 98715feb-2cad-48ca-a2a5-3d757a977d11
                Copyright © © The Author(s) 2019
                License:

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 24 December 2018
                Date revision received : 13 March 2019
                Date accepted : 19 March 2019
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100001809, National Natural Science Foundation of China (National Science Foundation of China);
                Award ID: 81172824
                Award Recipient :
                Categories
                Subject: Review Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2019

                ScienceOpen disciplines: Cell biology
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                ScienceOpen disciplines: Cell biology

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