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 ◽  
...  
2017 ◽  
Vol 140 (4) ◽  
pp. 1156-1159.e7 ◽  
Author(s):  
Shuo Li ◽  
Hideaki Morita ◽  
Beate Rückert ◽  
Tadech Boonpiyathad ◽  
Avidan Neumann ◽  
...  

2016 ◽  
Vol 9 (426) ◽  
pp. ra46-ra46 ◽  
Author(s):  
Charlotte Viant ◽  
Lucille C. Rankin ◽  
Mathilde J. H. Girard-Madoux ◽  
Cyril Seillet ◽  
Wei Shi ◽  
...  

2019 ◽  
Vol 15 (12) ◽  
pp. e1008140 ◽  
Author(s):  
Deepak Tripathi ◽  
Rajesh Kumar Radhakrishnan ◽  
Ramya Sivangala Thandi ◽  
Padmaja Paidipally ◽  
Kamakshi Prudhula Devalraju ◽  
...  

2016 ◽  
Vol 115 ◽  
pp. 81
Author(s):  
Derek Miller ◽  
Roberto Romero ◽  
Yi Xu ◽  
Sonia Hassan ◽  
Nardhy Gomez-Lopez

2016 ◽  
Vol 115 ◽  
pp. 35
Author(s):  
Derek Miller ◽  
Roberto Romero ◽  
Yi Xu ◽  
Sonia Hassan ◽  
Nardhy Gomez-Lopez

2015 ◽  
Vol 212 (11) ◽  
pp. 1783-1791 ◽  
Author(s):  
Patricia Aparicio-Domingo ◽  
Monica Romera-Hernandez ◽  
Julien J. Karrich ◽  
Ferry Cornelissen ◽  
Natalie Papazian ◽  
...  

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.


2015 ◽  
Vol 210 (7) ◽  
pp. 2107OIA193
Author(s):  
Patricia Aparicio-Domingo ◽  
Monica Romera-Hernandez ◽  
Julien J. Karrich ◽  
Ferry Cornelissen ◽  
Natalie Papazian ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Ana Valle-Noguera ◽  
Anne Ochoa-Ramos ◽  
Maria José Gomez-Sánchez ◽  
Aranzazu Cruz-Adalia

Type 3 Innate lymphoid cells (ILC3s) have been described as tissue-resident cells and characterized throughout the body, especially in mucosal sites and classical first barrier organs such as skin, gut and lungs, among others. A significant part of the research has focused on their role in combating pathogens, mainly extracellular pathogens, with the gut as the principal organ. However, some recent discoveries in the field have unveiled their activity in other organs, combating intracellular pathogens and as part of the response to viruses. In this review we have compiled the latest studies on the role of ILC3s and the molecular mechanisms involved in defending against different microbes at the mucosal surface, most of these studies have made use of conditional transgenic mice. The present review therefore attempts to provide an overview of the function of ILC3s in infections throughout the body, focusing on their specific activity in different organs.


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