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      Type 2 Innate Lymphocytes Actuate Immunity Against Tumours and Limit Cancer Metastasis

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          Abstract

          Type 2 innate lymphoid cells (ILC2) potentiate immune responses, however, their role in mediating adaptive immunity in cancer has not been assessed. Here, we report that mice genetically lacking ILC2s have significantly increased tumour growth rates and conspicuously higher frequency of circulating tumour cells (CTCs) and resulting metastasis to distal organs. Our data support the model that IL-33 dependent tumour-infiltrating ILC2s are mobilized from the lungs and other tissues through chemoattraction to enter tumours, and subsequently mediate tumour immune-surveillance by cooperating with dendritic cells to promote adaptive cytolytic T cell responses. We conclude that ILC2s play a fundamental, yet hitherto undescribed role in enhancing anti-cancer immunity and controlling tumour metastasis.

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          Distinct role of macrophages in different tumor microenvironments.

          Claire Lewis, Jeffrey W Pollard (2006)
          Macrophages are prominent in the stromal compartment of virtually all types of malignancy. These highly versatile cells respond to the presence of stimuli in different parts of tumors with the release of a distinct repertoire of growth factors, cytokines, chemokines, and enzymes that regulate tumor growth, angiogenesis, invasion, and/or metastasis. The distinct microenvironments where tumor-associated macrophages (TAM) act include areas of invasion where TAMs promote cancer cell motility, stromal and perivascular areas where TAMs promote metastasis, and avascular and perinecrotic areas where hypoxic TAMs stimulate angiogenesis. This review will discuss the evidence for differential regulation of TAMs in these microenvironments and provide an overview of current attempts to target or use TAMs for therapeutic purposes.
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            T cell receptor antagonist peptides induce positive selection.

            Kristin A. Hogquist, Stephen C. Jameson, William R. Heath … (1994)
            We have used organ culture of fetal thymic lobes from T cell receptor (TCR) transgenic beta 2M(-/-) mice to study the role of peptides in positive selection. The TCR used was from a CD8+ T cell specific for ovalbumin 257-264 in the context of Kb. Several peptides with the ability to induce positive selection were identified. These peptide-selected thymocytes have the same phenotype as mature CD8+ T cells and can respond to antigen. Those peptides with the ability to induce positive selection were all variants of the antigenic peptide and were identified as TCR antagonist peptides for this receptor. One peptide tested, E1, induced positive selection on the beta 2M(-/-) background but negative selection on the beta 2M(+/-) background. These results show that the process of positive selection is exquisitely peptide specific and sensitive to extremely low ligand density and support the notion that low efficacy ligands mediate positive selection.
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              Type 2 innate lymphoid cells control eosinophil homeostasis

              Jesse C. Nussbaum, Steven Van Dyken, Jakob von Moltke … (2013)
              Eosinophils are specialized myeloid cells associated with allergy and helminth infections. Blood eosinophils demonstrate circadian cycling, as described over 80 years ago, 1 and are abundant in the healthy gastrointestinal tract. Although a cytokine, interleukin (IL)-5, and chemokines such as eotaxins, mediate eosinophil development and survival, 2 and tissue recruitment, 3 respectively, the processes underlying the basal regulation of these signals remain unknown. Here, we show that serum IL-5 is maintained by long-lived type 2 innate lymphoid cells (ILC2) resident in peripheral tissues. ILC2 secrete IL-5 constitutively and are induced to co-express IL-13 during type 2 inflammation, resulting in localized eotaxin production and eosinophil accumulation. In the small intestine where eosinophils and eotaxin are constitutive, 4 ILC2 co-express IL-5 and IL-13, which is enhanced after caloric intake. The circadian synchronizer vasoactive intestinal peptide (VIP) also stimulates ILC2 through the VPAC2 receptor to release IL-5, linking eosinophil levels with metabolic cycling. Tissue ILC2 regulate basal eosinophilopoiesis and tissue eosinophil accumulation through constitutive and stimulated cytokine expression, and this dissociated regulation can be tuned by nutrient intake and central circadian rhythms.
              Article 0 comments Cited 420 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Wilfred A. Jefferies:
                ORCID: http://orcid.org/0000-0002-7392-9852
                wilf@msl.ubc.ca
                Journal
                Journal ID (nlm-ta): Sci Rep
                Journal ID (iso-abbrev): Sci Rep
                Title: Scientific Reports
                Publisher: Nature Publishing Group UK (London )
                ISSN (Electronic): 2045-2322
                Publication date (Electronic): 13 February 2018
                Publication date PMC-release: 13 February 2018
                Publication date Collection: 2018
                Volume: 8
                Electronic Location Identifier: 2924
                Affiliations
                [1 ]ISNI 0000 0001 2288 9830, GRID grid.17091.3e, The Michael Smith Laboratories, , University of British Columbia, 301-2185 East Mall, ; Vancouver, V6T 1Z4 BC Canada
                [2 ]ISNI 0000 0004 0384 4428, GRID grid.417243.7, The Vancouver Prostate Centre, , Vancouver Coastal Health Research Institute, ; Vancouver, Canada
                [3 ]ISNI 0000 0001 2288 9830, GRID grid.17091.3e, Department of Microbiology & Immunology, , University of British Columbia, ; Vancouver, Canada
                [4 ]ISNI 0000 0001 2288 9830, GRID grid.17091.3e, Department of Animal Care Services, , University of British Columbia, ; Vancouver, Canada
                [5 ]ISNI 0000 0001 0702 3000, GRID grid.248762.d, Terry Fox Laboratory, BC Cancer Agency, ; Vancouver, Canada
                [6 ]ISNI 0000 0001 2288 9830, GRID grid.17091.3e, Department of Pathology & Laboratory Medicine, , University of British Columbia, ; Vancouver, Canada
                [7 ]ISNI 0000 0001 2288 9830, GRID grid.17091.3e, Department of Medical Genetics, , University of British Columbia, ; Vancouver, Canada
                [8 ]ISNI 0000 0001 2288 9830, GRID grid.17091.3e, Department of Zoology, , University of British Columbia, ; Vancouver, Canada
                [9 ]ISNI 0000 0001 2288 9830, GRID grid.17091.3e, The Centre for Blood Research, , University of British Columbia, ; Vancouver, Canada
                [10 ]ISNI 0000 0001 2288 9830, GRID grid.17091.3e, Djavad Mowafaghian Centre for Brain Health, , University of British Columbia, ; Vancouver, Canada
                Author information
                http://orcid.org/0000-0002-0007-4128
                http://orcid.org/0000-0002-7392-9852
                Article
                Publisher ID: 20608
                DOI: 10.1038/s41598-018-20608-6
                PMC ID: 5811448
                PubMed ID: 29440650
                SO-VID: 7ad9c9e9-6753-4826-bd38-992bf1f67618
                Copyright © © The Author(s) 2018
                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 : 4 July 2017
                Date accepted : 15 January 2018
                Categories
                Subject: Article
                Custom metadata
                issue-copyright-statement © The Author(s) 2018

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