Abstract
During the early phase of an inflammatory response, innate cells can use different strategies to sense environmental danger. These include the direct interaction of specific activating receptors with pathogen-encoded/danger molecules or the engagement of cytokine receptors by pro-inflammatory mediators produced by antigen presenting cells in the course of the infection. These general recognition strategies, which have been extensively described for innate myeloid cells, are shared by innate lymphoid cells (ILC), such as Natural Killer (NK) cells. The family of ILC has recently expanded with the discovery of group 2 (ILC2) and group 3 ILC (ILC3), which play an important role in the defense against extracellular pathogens. Although ILC3 and NK cells share some phenotypic characteristics, the recognition strategies employed by the various ILC3 subsets have been only partially characterized. In this review, we will describe and comparatively discuss how ILC3 sense environmental cues and how the triggering of different receptors may regulate their functional behavior during an immune response.
Highlights
Innate lymphoid cells (ILC) represent a family of innate effectors lacking recombination activating gene (RAG)-dependent rearranged antigen receptors and myeloid and dendritic cell (DC) markers
While the recognition strategies employed by Natural Killer (NK) cells have been extensively investigated, the analysis of the receptors mediating the activation of ILC3 and ILC2 is still at the beginning
In one of the first reports, human IL-22producing RORγt+ ILC3 were identified as Lin− CD56+ NKp44+ cells and termed NK-22 [16], tonsil and gut lamina propria (LP) CD56− NKp44+ and CD56+ NKp44− cells are enriched in RORC transcripts
Summary
Innate lymphoid cells (ILC) represent a family of innate effectors lacking recombination activating gene (RAG)-dependent rearranged antigen receptors and myeloid and dendritic cell (DC) markers. In one of the first reports, human IL-22producing RORγt+ ILC3 were identified as Lin− CD56+ NKp44+ cells and termed NK-22 [16], tonsil and gut LP CD56− NKp44+ and CD56+ NKp44− cells are enriched in RORC transcripts. Other reports have recently outlined the importance of IL-17A and IL-17F production by ILC3 for the protection against mucosal Candida infections [59] Due to their ability to modulate epithelial cell functions as well as to respond against commensal bacteria and pathogens, ILC3 participate in the complex regulation of inflammatory bowel disease (IBD), displaying rather a dual role.
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