Functional and phenotypic heterogeneity of group 3 innate lymphoid cells
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- Felipe Melo‐Gonzalez
- Faculty of Biology Medicine and Health School of Biological Sciences Division of Infection, Immunity and Respiratory Medicine University of Manchester Manchester UK
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- Matthew R. Hepworth
- Faculty of Biology Medicine and Health School of Biological Sciences Division of Infection, Immunity and Respiratory Medicine University of Manchester Manchester UK
Description
<jats:title>Summary</jats:title><jats:p>Group 3 innate lymphoid cells (<jats:styled-content style="fixed-case">ILC</jats:styled-content>3), defined by expression of the transcription factor retinoid‐related orphan receptor <jats:italic>γ</jats:italic>t, play key roles in the regulation of inflammation and immunity in the gastrointestinal tract and associated lymphoid tissues. <jats:styled-content style="fixed-case">ILC</jats:styled-content>3 consist largely of two major subsets, <jats:styled-content style="fixed-case">NCR</jats:styled-content><jats:sup>+</jats:sup> <jats:styled-content style="fixed-case">ILC</jats:styled-content>3 and <jats:styled-content style="fixed-case">LT</jats:styled-content>i‐like <jats:styled-content style="fixed-case">ILC</jats:styled-content>3, but also demonstrate significant plasticity and heterogeneity. Recent advances have begun to dissect the relationship between <jats:styled-content style="fixed-case">ILC</jats:styled-content>3 subsets and to define distinct functional states within the intestinal tissue microenvironment. In this review we discuss the ever‐expanding roles of <jats:styled-content style="fixed-case">ILC</jats:styled-content>3 in the context of intestinal homeostasis, infection and inflammation – with a focus on comparing and contrasting the relative contributions of <jats:styled-content style="fixed-case">ILC</jats:styled-content>3 subsets.</jats:p>
Journal
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- Immunology
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Immunology 150 (3), 265-275, 2017-01-03
Wiley
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Details 詳細情報について
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- CRID
- 1363670318663874688
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- ISSN
- 13652567
- 00192805
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- Data Source
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- Crossref