Innate lymphoid cells type 3 are increased in spontaneous preterm labor

2016 ◽  
Vol 115 ◽  
pp. 81
Author(s):  
Derek Miller ◽  
Roberto Romero ◽  
Yi Xu ◽  
Sonia Hassan ◽  
Nardhy Gomez-Lopez
Keyword(s):  
Preterm Labor ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Type 3

Innate Lymphoid Cells Type 3 are Increased in Spontaneous Preterm Labor

2016 ◽  
Vol 115 ◽  
pp. 35
Author(s):  
Derek Miller ◽  
Roberto Romero ◽  
Yi Xu ◽  
Sonia Hassan ◽  
Nardhy Gomez-Lopez
Keyword(s):  
Preterm Labor ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Type 3

scholarly journals Type 3 innate lymphoid cells induce proliferation of CD94+ natural killer cells

2017 ◽  
Vol 140 (4) ◽  
pp. 1156-1159.e7 ◽  
Author(s):  
Shuo Li ◽  
Hideaki Morita ◽  
Beate Rückert ◽  
Tadech Boonpiyathad ◽  
Avidan Neumann ◽  
...  
Keyword(s):  
Natural Killer Cells ◽  
Natural Killer ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Killer Cells ◽  
Type 3

Transforming growth factor–β and Notch ligands act as opposing environmental cues in regulating the plasticity of type 3 innate lymphoid cells

2016 ◽  
Vol 9 (426) ◽  
pp. ra46-ra46 ◽  
Author(s):  
Charlotte Viant ◽  
Lucille C. Rankin ◽  
Mathilde J. H. Girard-Madoux ◽  
Cyril Seillet ◽  
Wei Shi ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Environmental Cues ◽  
Type 3 ◽  
Notch Ligands

scholarly journals IL-22 produced by type 3 innate lymphoid cells (ILC3s) reduces the mortality of type 2 diabetes mellitus (T2DM) mice infected with Mycobacterium tuberculosis

2019 ◽  
Vol 15 (12) ◽  
pp. e1008140 ◽  
Author(s):  
Deepak Tripathi ◽  
Rajesh Kumar Radhakrishnan ◽  
Ramya Sivangala Thandi ◽  
Padmaja Paidipally ◽  
Kamakshi Prudhula Devalraju ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mycobacterium Tuberculosis ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Type 3

scholarly journals Glial-cell-derived neuroregulators control type 3 innate lymphoid cells and gut defence

Nature ◽  
2016 ◽  
Vol 535 (7612) ◽  
pp. 440-443 ◽  
Author(s):  
Sales Ibiza ◽  
Bethania García-Cassani ◽  
Hélder Ribeiro ◽  
Tânia Carvalho ◽  
Luís Almeida ◽  
...  
Keyword(s):  
Glial Cell ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Type 3

scholarly journals Type 3 innate lymphoid cells maintain intestinal epithelial stem cells after tissue damage

2015 ◽  
Vol 212 (11) ◽  
pp. 1783-1791 ◽  
Author(s):  
Patricia Aparicio-Domingo ◽  
Monica Romera-Hernandez ◽  
Julien J. Karrich ◽  
Ferry Cornelissen ◽  
Natalie Papazian ◽  
...  
Keyword(s):  
Stem Cells ◽  
Tissue Damage ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Intestinal Damage ◽  
Intestinal Epithelial ◽  
Epithelial Stem Cells ◽  
Intestinal Tissue ◽  
Mucosal Surfaces ◽  
Type 3

Disruption of the intestinal epithelial barrier allows bacterial translocation and predisposes to destructive inflammation. To ensure proper barrier composition, crypt-residing stem cells continuously proliferate and replenish all intestinal epithelial cells within days. As a consequence of this high mitotic activity, mucosal surfaces are frequently targeted by anticancer therapies, leading to dose-limiting side effects. The cellular mechanisms that control tissue protection and mucosal healing in response to intestinal damage remain poorly understood. Type 3 innate lymphoid cells (ILC3s) are regulators of homeostasis and tissue responses to infection at mucosal surfaces. We now demonstrate that ILC3s are required for epithelial activation and proliferation in response to small intestinal tissue damage induced by the chemotherapeutic agent methotrexate. Multiple subsets of ILC3s are activated after intestinal tissue damage, and in the absence of ILC3s, epithelial activation is lost, correlating with increased pathology and severe damage to the intestinal crypts. Using ILC3-deficient Lgr5 reporter mice, we show that maintenance of intestinal stem cells after damage is severely impaired in the absence of ILC3s or the ILC3 signature cytokine IL-22. These data unveil a novel function of ILC3s in limiting tissue damage by preserving tissue-specific stem cells.

scholarly journals Type 3 innate lymphoid cells maintain intestinal epithelial stem cells after tissue damage

2015 ◽  
Vol 210 (7) ◽  
pp. 2107OIA193
Author(s):  
Patricia Aparicio-Domingo ◽  
Monica Romera-Hernandez ◽  
Julien J. Karrich ◽  
Ferry Cornelissen ◽  
Natalie Papazian ◽  
...  
Keyword(s):  
Stem Cells ◽  
Tissue Damage ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Intestinal Epithelial ◽  
Epithelial Stem Cells ◽  
Type 3

scholarly journals Innate lymphoid cells at the maternal-fetal interface: Implications in preterm labor

2019 ◽  
Author(s):  
João Fernando Pereira Mendes ◽  
Paulo Rodrigues Santos ◽  
Ana Areia ◽  
Jani Sofia Almeida ◽  
Vera Alves ◽  
...  
Keyword(s):  
Preterm Labor ◽  
Group Analysis ◽  
Neonatal Morbidity ◽  
Innate Lymphoid Cells ◽  
Lymphoid Cells ◽  
Data Set ◽  
Proinflammatory Mediators ◽  
Maternal Peripheral Blood ◽  
Human Labor ◽  
Maternal Fetal Interface

Abstract Background: Preterm labor (PTL) is one of the major causes of neonatal morbidity and mortality worldwide. It is commonly accepted that the act of giving birth is the final step in a proinflammatory signaling cascade, orchestrated by an intrauterine milieu coupled to hormonal cues. Consequently, the inflammatory process plays a pivotal role during the pathogenesis of human labor, both in term and preterm deliveries. The aim of this work was to analyze the abilities of innate lymphoid cells (ILCs), specifically ILC3 NCR- cells, to act as proinflammatory mediators and to elucidate their role in pregnancy. Accordingly, we hypothesize that altered ILC numbers may prompt preterm labor (PTL). Methods: We analyzed thirteen full term labor (FTL) and seven PTL pregnant women for the presence of ILCs. ILCs were isolated and characterized from maternal peripheral blood, maternal-fetal interface, and cord blood samples, using flow cytometry. For group analysis, two-way ANOVA was performed. Each data set was analyzed using student t-test with a confidence interval of 95%. Results: A tendency for decreased ILCs numbers in PTL samples compared to those in FTL samples was observed. Additionally, ILC3 NCR- cells were significantly increased in both PTL and FTL groups, when compared to ILC3NCR+. Conclusion: Our results support a potential inflammatory role of ILC3 NCR- in the instigation of labor. Moreover our work highlights the importance of ILCs actions in the regulation of labor.

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