Faculty Opinions recommendation of Group 3 innate lymphoid cells regulate neutrophil migration and function in human decidua.

2019 ◽  
Author(s):  
Gendie Lash
Keyword(s):  
Neutrophil Migration ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Group 3 ◽  
And Function ◽  
Human Decidua

scholarly journals Group 3 innate lymphoid cells regulate neutrophil migration and function in human decidua

2016 ◽  
Vol 9 (6) ◽  
pp. 1372-1383 ◽  
Author(s):  
D Croxatto ◽  
A Micheletti ◽  
E Montaldo ◽  
P Orecchia ◽  
F Loiacono ◽  
...  
Keyword(s):  
Neutrophil Migration ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Group 3 ◽  
And Function ◽  
Human Decidua

scholarly journals An Anti-inflammatory microRNA Signature Distinguishes Group 3 Innate Lymphoid Cells From Natural Killer Cells in Human Decidua

2020 ◽  
Vol 11 ◽  
Author(s):  
Andrea Pelosi ◽  
Claudia Alicata ◽  
Nicola Tumino ◽  
Tiziano Ingegnere ◽  
Fabrizio Loiacono ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Natural Killer ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Killer Cells ◽  
Group 3 ◽  
Anti Inflammatory ◽  
Human Decidua

scholarly journals PD-1 is expressed by and regulates human group 3 innate lymphoid cells in human decidua

2019 ◽  
Vol 12 (3) ◽  
pp. 624-631 ◽  
Author(s):  
Paola Vacca ◽  
Silvia Pesce ◽  
Marco Greppi ◽  
Ezio Fulcheri ◽  
Enrico Munari ◽  
...  
Keyword(s):  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Human Group ◽  
Group 3 ◽  
Human Decidua

scholarly journals c-Maf regulates the plasticity of group 3 innate lymphoid cells by restraining the type 1 program

2019 ◽  
Vol 217 (1) ◽  
Author(s):  
Morgan E. Parker ◽  
Alejandro Barrera ◽  
Joshua D. Wheaton ◽  
Matthew K. Zuberbuehler ◽  
David S.J. Allan ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Innate Lymphoid Cells ◽  
Chromatin Accessibility ◽  
Lymphoid Cells ◽  
Global Changes ◽  
Intestinal Immunity ◽  
Phenotypic Analysis ◽  
Group 3 ◽  
And Function

CCR6− group 3 innate lymphoid cells (ILC3s) are mediators of intestinal immunity and barrier function that possess the capacity to acquire type 1 effector features and fully convert into ILC1s. The molecular mechanisms governing such plasticity are undefined. Here, we identified c-Maf as an essential regulator of ILC3 homeostasis and plasticity that limits physiological ILC1 conversion. Phenotypic analysis of effector status in Maf-deficient CCR6− ILC3s, coupled with evaluation of global changes in transcriptome, chromatin accessibility, and transcription factor motif enrichment, revealed that c-Maf enforces ILC3 identity. c-Maf promoted ILC3 accessibility and supported RORγt activity and expression of type 3 effector genes. Conversely, c-Maf antagonized type 1 programming, largely through restraint of T-bet expression and function. Mapping of the dynamic changes in chromatin landscape accompanying CCR6− ILC3 development and ILC1 conversion solidified c-Maf as a gatekeeper of type 1 regulatory transformation and a controller of ILC3 fate.

scholarly journals DOCK8 controls survival of group 3 innate lymphoid cells in the gut through Cdc42 activation

2020 ◽  
Author(s):  
Ryosuke Aihara ◽  
Kazufumi Kunimura ◽  
Mayuki Watanabe ◽  
Takehito Uruno ◽  
Nana Yamane ◽  
...  
Keyword(s):  
Fetal Liver ◽  
Underlying Mechanism ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Brdu Incorporation ◽  
Catalytic Center ◽  
Dock8 Deficiency ◽  
Group 3 ◽  
And Function

Abstract Innate lymphoid cells (ILCs) are a family of developmentally related leukocytes that rapidly secrete polarized sets of cytokines to combat infection and promote tissue repair at mucosal barriers. Among them, group 3 ILCs (ILC3s) play an important role in maintenance of the gut homeostasis by producing IL-22, and their development and function critically depend on the transcription factor RORγt. Although recent evidence indicates that RORγt+ ILC3s are reduced in the gut in the absence of the Cdc42 activator DOCK8 (dedicator of cytokinesis 8), the underlying mechanism remains unclear. We found that genetic deletion of Dock8 in RORγt+-lineage cells markedly reduced ILC3s in the lamina propria of the small intestine. By analyzing BrdU incorporation, it was revealed that DOCK8 deficiency did not affect the cell proliferation. Furthermore, when lineage marker-negative (Lin–) α4β7+ CD127+ RORγt– fetal liver cells were cultured with OP9 stromal cells in the presence of stem cell factor (SCF) and IL-7 in vitro, RORγt+ ILC3s normally developed irrespective of DOCK8 expression. However, DOCK8-deficient ILC3s exhibited a severe defect in survival of ILC3s under the condition with or without IL-7. Similar defects were observed when we analyzed Dock8VAGR mice having mutations in the catalytic center of DOCK8, thereby failing to activate Cdc42. Thus, DOCK8 acts in cell-autonomous manner to control survival of ILC3s in the gut through Cdc42 activation.

scholarly journals The Role of Group 3 Innate Lymphoid Cells in Lung Infection and Immunity

2021 ◽  
Vol 11 ◽  
Author(s):  
Dan Yang ◽  
Xinning Guo ◽  
Tingxuan Huang ◽  
Chuntao Liu
Keyword(s):  
Respiratory Infections ◽  
Inflammatory Diseases ◽  
Pulmonary Inflammation ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Intestinal Immunity ◽  
Group 3 ◽  
Underlying Mechanisms ◽  
And Function ◽  
Pathogen Clearance

The lung is constantly exposed to environmental particulates such as aeroallergens, pollutants, or microorganisms and is protected by a poised immune response. Innate lymphoid cells (ILCs) are a population of immune cells found in a variety of tissue sites, particularly barrier surfaces such as the lung and the intestine. ILCs play a crucial role in the innate immune system, and they are involved in the maintenance of mucosal homeostasis, inflammation regulation, tissue remodeling, and pathogen clearance. In recent years, group 3 innate lymphoid cells (ILC3s) have emerged as key mediators of mucosal protection and repair during infection, mainly through IL-17 and IL-22 production. Although research on ILC3s has become focused on the intestinal immunity, the biology and function of pulmonary ILC3s in the pathogenesis of respiratory infections and in the development of chronic pulmonary inflammatory diseases remain elusive. In this review, we will mainly discuss how pulmonary ILC3s act on protection against pathogen challenge and pulmonary inflammation, as well as the underlying mechanisms.

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