ILC1 Confer Early Host Protection at Initial Sites of Viral Infection

Weizman, Orr-El; Adams, Nicholas M.; Schuster, Iona S.; Krishna, Chirag; Pritykin, Yuri; Lau, Colleen M.; Degli-Esposti, Mariapia A.; Leslie, Christina; Sun, Joseph C.; O’Sullivan, Timothy E.

doi:10.1016/j.cell.2017.09.052

Cited by 380 publications

(493 citation statements)

References 64 publications

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“…Despite only representing a minor fraction of total ILCs in the lung, 58,64 there is evidence that ILC1s play a role in immunosurveillance and infection control. 66 In both studies, ILC1s are probably responding to IL-12 or IL-18 produced by lung-resident dendritic cell (DC) subsets. The concept of ILC1s as important early producers of IFN-c in tissue is supported by a recent study showing depletion of ILC1s from Tcell-deficient mice increased titres of another respiratory virus, Sendai virus in the lung following nasal challenge.…”

Section: Innate Lymphoid Cellsmentioning

confidence: 99%

Tissue‐resident innate immunity in the lung

2019

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The lung is a unique organ that must protect against inhaled pathogens and toxins, without mounting a disproportionate response against harmless particulate matter and without compromising its vital function. Tissue-resident immune cells within the lung provide local immunity and protection from infection but are also responsible for causing disease when dysregulated. There is a growing appreciation of the importance of tissue-resident memory T cells to lung immunity, but non-recirculating, tissue-resident, innate immune cells also exist. These cells provide the first line of defence against pulmonary infection and are essential for co-ordinating the subsequent adaptive response. In this review, we discuss the main lung-resident innate immune subsets and their functions in common pulmonary diseases, such as influenza, bacterial pneumonia, asthma and inflammatory disorders.

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Section: Innate Lymphoid Cellsmentioning

confidence: 99%

Tissue‐resident innate immunity in the lung

2019

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“…ILC1 produce TNF and IFN‐γ but are poorly cytotoxic. Their broad physiological functions remain to be deciphered but recent studies have shown an involvement in the response to intracellular pathogens (such as Toxoplasma gondii ) and in immunity to tumors and viruses . ILC2 fate is governed by GATA3 and BCL11b .…”

Section: Introductionmentioning

confidence: 99%

A catch‐22: Interleukin‐22 and cancer

2018

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Barrier surfaces of multicellular organisms are in constant contact with the environment and infractions to the integrity of epithelial surfaces is likely a frequent event. Interestingly, components of the immune system, that can be activated by environmental compounds such as the microbiota or nutrients, are interspersed among epithelial cells or directly underlie the epithelium. It is now appreciated that immune cells continuously receive and integrate signals from the environment. Curiously, such continuous reception of stimulation does not normally trigger an inflammatory response but mediators produced by immune cells in response to such signals seem to rather promote barrier integrity and repair. The molecular mediators involved in this process are poorly understood. In recent years, the cytokine interleukin-22, produced mainly by group 3 innate lymphoid cells (ILCs), has been studied as a paradigm for how immune cells can control various aspects of epithelial cell function because expression of its receptor is restricted to non-hematopoietic cells. We will summarize here the diverse roles of IL-22 for the malignant transformation of epithelial cells, for tumor growth, wound healing and tissue repair. Furthermore, we will discuss IL-22 as a potential therapeutic target. Keywords:Aryl hydrocarbon receptor r Cancer r IL-22 r Innate lymphoid cells r RORγt IntroductionBarrier organs like the skin, the gut and lung mucosae are in constant contact with the environment. Their cellular components need to adapt to the continuous and ever changing presence of a large number of microbes (i.e., bacteria, fungi, viruses and parasites collectively referred to as the "microbiome") and their metabolites, including toxins. In addition, the epithelial barrier of the intestine is also subjected to food components, some of which are toxic by being poisonous, noxious or irritating. The skin barrier is exposed to UV irradiation, which is beneficial (e.g., conversion of Vitamin D) but can also be harmful (e.g., direct and Correspondence: Dr. Andreas Diefenbach e-mail: andreas.diefenbach@charite.de indirect DNA damage). Thus, barrier surfaces with the environment are sites where adaptive processes are initiated. Over millions of years of co-evolution of multicellular organisms with their habitat, adaptive signaling networks have been selected that are believed to shield the organism against such continuous threats and, thereby, shape their fitness. A well-studied example of such adaptive processes is microbiota-host relationships [1]. Through contact with microbial communities, epithelial function is being modified as to minimize damage to the barrier. For example, epithelial cells directly receive signals from the microbiota leading to the production of anti-bacterial proteins and to the protection of epithelial cells against TNF-triggered apoptosis [2][3][4]. * These authors contributed equally to this work.C 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim www.eji-journal.eu 16Pedro Hernandez et al. Eur. J. Immunol. 2018. 48: ...

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“…Despite this, we did not observe any alterations in cytokine‐producing capacity of the cNK cell populations, suggesting that the functionality of these cells remains intact. It was interesting to note that the absence of H2‐Q10 did not affect the maturation of ILC‐1, given that these cells are liver‐restricted while the cNK cells are not (Figure ) . As such, it would be expected that ILC‐1 would be more consistently exposed to Qa‐1b and the associated reduction in its expression in H2‐Q10‐deficient mice.…”

Section: Discussionmentioning

confidence: 98%

Multiple receptors converge on H2‐Q10 to regulate NK and γδT‐cell development

et al. 2019

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Class Ib major histocompatibility complex (MHC) is an extended family of molecules, which demonstrate tissue‐specific expression and presentation of monomorphic antigens. These characteristics tend to imbue class Ib MHC with unique functions. H2‐Q10 is potentially one such molecule that is overexpressed in the liver but its immunological function is not known. We have previously shown that H2‐Q10 is a ligand for the natural killer cell receptor Ly49C and now, using H2‐Q10‐deficient mice, we demonstrate that H2‐Q10 can also stabilize the expression of Qa‐1b. In the absence of H2‐Q10, the development and maturation of conventional hepatic natural killer cells is disrupted. We also provide evidence that H2‐Q10 is a new high affinity ligand for CD8αα and controls the development of liver‐resident CD8αα γδT cells. These data demonstrate that H2‐Q10 has multiple roles in the development of immune subsets and identify an overlap of recognition within the class Ib MHC that is likely to be relevant to the regulation of immunity.

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ILC1 Confer Early Host Protection at Initial Sites of Viral Infection

Cited by 380 publications

References 64 publications

Tissue‐resident innate immunity in the lung

Tissue‐resident innate immunity in the lung

A catch‐22: Interleukin‐22 and cancer

Multiple receptors converge on H2‐Q10 to regulate NK and γδT‐cell development

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