IL-22-Producing RORγt-Dependent Innate Lymphoid Cells Play a Novel Protective Role in Murine Acute Hepatitis

Matsumoto, Atsuhiro; Kanai, Takanori; Mikami, Yohei; Chu, Po–Sung; Nakamoto, Nobuhiro; Ebinuma, Hirotoshi; Saito, Hidetsugu; Sato, Toshiro; Yagita, Hideo; Hibi, Toshifumi

doi:10.1371/journal.pone.0062853

Cited by 32 publications

(31 citation statements)

References 27 publications

(62 reference statements)

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“…IL-22 acts on thymic epithelial cells to promote cell survival and proliferation 92 . Further, IL-22-dependent tissue repair in mice has also been reported in the liver following chemical-induced hepatitis 79 and lung following influenza infection or bleomycin-induced damage 87,93,94 , which are two other organs where the tissue resident non-hematopoietic cells highly express the IL-22 receptor 8 .…”

Section: Ilcs Promote the Resolution Of Inflammation And Tissue Repairmentioning

confidence: 94%

Innate lymphoid cells in the initiation, regulation and resolution of inflammation

Sonnenberg¹,

Artis²

2015

Nat Med

433

397

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A previously unappreciated cell type of the innate immune system, termed innate lymphoid cells (ILCs), has been characterized in mice and humans, and found to profoundly influence the induction, regulation and resolution of inflammation. ILCs play an important role in these processes in murine models of infection, inflammatory disease and tissue repair. Further, disease association studies in defined patient populations have identified significant alterations in ILC responses, suggesting a potential role for these cell populations in human health and disease. In this review, we discuss the emerging family of ILCs, the role of ILCs in inflammation, and how current or novel therapeutic strategies could be employed to selectively modulate ILC responses and limit chronic inflammatory diseases in patients.

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Section: Ilcs Promote the Resolution Of Inflammation And Tissue Repairmentioning

confidence: 94%

Innate lymphoid cells in the initiation, regulation and resolution of inflammation

Sonnenberg¹,

Artis²

2015

Nat Med

433

397

View full text Add to dashboard Cite

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“…After damage to the thymus, as seen after whole‐body irradiation, radio‐resistant ILC3 support thymus regeneration by the secretion of IL‐22 . ILC3‐derived IL‐22 is also an important driver in liver tissue repair after chemically induced hepatitis …”

Section: Ilc As Guardians Of Tissue Homeostasis Epithelial Remodelinmentioning

confidence: 99%

Innate lymphoid cells, mediators of tissue homeostasis, adaptation and disease tolerance

Branzk

Gronke

Diefenbach

2018

Immunological Reviews

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Summary Innate lymphoid cells (ILC) are a recently identified group of tissue‐resident innate lymphocytes. Available data support the view that ILC or their progenitors are deposited and retained in tissues early during ontogeny. Thereby, ILC become an integral cellular component of tissues and organs. Here, we will review the intriguing relationships between ILC and basic developmental and homeostatic processes within tissues. Studying ILC has already led to the appreciation of the integral roles of immune cells in tissue homeostasis, morphogenesis, metabolism, regeneration, and growth. This area of immunology has not yet been studied in‐depth but is likely to reveal important networks contributing to disease tolerance and may be harnessed for future therapeutic approaches.

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“…In the last several years, ILCs have been found to be involved in innate immunity as well as tissue remodeling (32). In the liver, ILCs have been shown to protect against acute hepatitis (33, 34), but can also mediate hepatic fibrosis (35). In addition, we found that IL-17 signaling was important for adaptive T cell responses in viral hepatitis.…”

Section: Introductionmentioning

confidence: 99%

Intrahepatic Innate Lymphoid Cells Secrete IL-17A and IL-17F That Are Crucial for T Cell Priming in Viral Infection

Jie

Liang

Hou

et al. 2014

The Journal of Immunology

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Intrahepatic cell-derived, early IL-17 is important for activating antigen-presenting cells in viral infection; however, the source and regulation of this IL-17 surge in the liver microenvironment are not well defined. Here, we present evidence for a significant expansion of IL-17A/F-producing cells in mouse liver within 24 h of adenovirus (Ad) infection. In addition to λδ T cells, a subset of IL-17A/F+ cells expressed no myeloid or lymphoid lineage markers. Instead, they expressed high levels of stem cell markers, IL-7 receptor and RORλt, consistent with the newly described innate lymphoid cells. Based on their unique surface markers and cytokine profiles, these cells were confirmed as group 3 innate lymphoid cells (ILC3s). In addition to Ad infection, ILC3s were also found in mouse liver within 24 h of LCMV infection. They contributed significantly to the establishment of the early cytokine milieu in virus-infected liver. Functional studies with mice deficient of IL-17 receptor, IL-17A, and IL-17F further revealed that IL-17 signaling was critical for priming T cell responses in viral hepatitis. IL-17A repressed IL-17F secretion in vitro and in vivo; IL-17F+ intrahepatic cells expanded more vigorously in IL-17A knockout animals, permitting efficient antigen-presentation and T cell function. However, IL-17F neither inhibited IL-17A in vitro, nor regulated its secretion in vivo. Together, this study has demonstrated the importance of a unique intrahepatic subpopulation and subsequent IL-17A/F regulation at initial stages of viral infection in the liver. These results have important implications for anti-cytokine biologic therapy and vaccine development.

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IL-22-Producing RORγt-Dependent Innate Lymphoid Cells Play a Novel Protective Role in Murine Acute Hepatitis

Cited by 32 publications

References 27 publications

Innate lymphoid cells in the initiation, regulation and resolution of inflammation

Innate lymphoid cells in the initiation, regulation and resolution of inflammation

Innate lymphoid cells, mediators of tissue homeostasis, adaptation and disease tolerance

Intrahepatic Innate Lymphoid Cells Secrete IL-17A and IL-17F That Are Crucial for T Cell Priming in Viral Infection

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