Abstract
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.
Highlights
Innate lymphoid cells (ILCs) are a subset of lymphocytes lacking the rearranged antigen receptors expressed by adaptive cells, and residing in peripheral tissues, at barrier surfaces
It has recently been determined that aryl hydrocarbon receptor (AhR) expression in receptor g t (RORgt)+ cells alone was sufficient with regard to maintaining a functional ILC3 compartment and controlling C. rodentium infection; this was demonstrated by the complete protection of AhrCAIR/CAIR Rorc Cre mice, an AhR-knockin mouse model that expressed a constitutively active form of AhR (CA-AhR) only in RORgt+ cells [104]
The present review addresses the latest studies on ILC3s in the early release of cytokines in various organs of the body in mice and humans - in particular the secretion of interleukin 17 (IL-17) and IL-22, and their role in the early response to a wide range of pathogens
Summary
Innate lymphoid cells (ILCs) are a subset of lymphocytes lacking the rearranged antigen receptors expressed by adaptive cells, and residing in peripheral tissues, at barrier surfaces. IL-17-producing ILC3s could be key players upon infection with G. lamblia [75] but further research studying this model in Rag−/− mice with the depletion of Il-17 gene in the RORgt+ cells is required to demonstrate this hypothesis.
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