IL-15 sustains IL-7R-independent ILC2 and ILC3 development

Robinette, Michelle L.; Bando, Jennifer K.; Song, Wilbur M.; Ulland, Tyler K.; Gilfillan, Susan; Colonna, Marco

doi:10.1038/ncomms14601

Cited by 103 publications

(97 citation statements)

References 51 publications

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“…Furthermore, ILC cross talk with activated T cells has been suggested by several studies 7,14,15 , arguing that disruption of T cell activation may impact upon ILC homeostasis. In addition, the cytokines that support ILC homeostasis, IL-7 and IL-15, are similarly required for T cell populations, and competition for these molecules has been proposed as a mechanism limiting ILC and T cell numbers 16,26 . Thus we considered that it would be informative to extend our analysis of ILC populations to mice deficient in both CD80 and CD86, where signals through CD28 are deficient and thus T cell activation is blocked ( Figure 5 A-C).…”

Section: Ilc Populations In Mice Lacking Activated T Cellsmentioning

confidence: 99%

“…Thus our aim was to extend this approach to compare ILC populations within a range of lymphoid and non-lymphoid tissues, reasoning that this would provide a useful resource from which to better develop understanding of ILC populations. Several studies have also indicated that ILC:T cell cross talk shapes the outcome of CD4 T cell responses 7,14,15 and that both cell types require common γ chain cytokines for their homeostasis [16][17][18] . Furthermore, ILCs express a number of costimulatory molecules whose expression is shared with T cells, although the role these molecules play in ILC function requires further investigation 3,19,20 .…”

Section: Introductionmentioning

confidence: 99%

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Characterisation of innate lymphoid cell populations at different sites in mice with defective T cell immunity

Dutton¹,

Camelo²,

Sleeman³

et al. 2017

Wellcome Open Res

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Innate lymphoid cells (ILCs) have now been identified within Background most tissues of the body and current evidence indicates that this family of cells play a fundamental role in maintaining tissue homeostasis. However, few studies have compared the ILC populations between several tissues.: We sought to generate a comprehensive characterisation of the ILC Methods populations in different tissues of C57BL/6 WT and genetically modified mice targeting costimulatory pathways, using transcription factor expression to define specific groups.: Consistent with studies individually describing the ILC composition in Results different tissues, our analysis revealed different ILC groups dominate the ILC population in different tissues. Additionally, we observed a population of IL-7Rα Id2 cells lacking expression of lineage markers but also lacking expression of GATA-3, RORgt or T-bet. This population was most evident in ear skin where it outnumbered the defined ILC groups, however, further experiments demonstrated that detection of these cells was influenced by how the tissue was digested, raising concerns as to its real nature. Since both ILC2 and ILC3 express ICOS, we then investigated the requirement for ICOS:ICOSL interactions in the homeostasis of ILC populations at these sites. Surprisingly, no significant differences were detected in the number of ILC1, ILC2 or ILC3 between WT and ICOSL mice in any tissue, indicating that this pathway is not required for ILC homeostasis at these sites. These data were compared with CD80 CD86 mice given evidence of CD28 expression by some ILC and ILC crosstalk with activated T cells. Notably, the absence of CD28 ligands resulted in a significant increase in ILC2 and ILC3 numbers in the intestine.: Together, these data provide new insight into ILC composition in Conclusions different tissues in both WT and genetically modified mice where key costimulatory pathways are genetically deleted, providing a useful resource for further research into ILC biology.

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Section: Ilc Populations In Mice Lacking Activated T Cellsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Characterisation of innate lymphoid cell populations at different sites in mice with defective T cell immunity

Dutton¹,

Camelo²,

Sleeman³

et al. 2017

Wellcome Open Res

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“…A possible explanation for this phenotype relies on a compensatory mechanism involving TSLP signals through IL‐7Rα, in the absence of IL‐7. However, persistence of selective ILC2 and ILC3 populations has also been observed in Il7ra −/− mice and the presence of these residual cells is partially sustained by IL‐15 . These studies highlight the possibility that beyond the “canonical” ILC development, compensatory cytokine switches may occur in selective microenvironments.…”

Section: Jak/stat Pathway In Ilc Biologymentioning

confidence: 76%

JAK/STAT signaling in regulation of innate lymphoid cells: The gods before the guardians

Stabile

Scarno

Fionda

et al. 2018

Immunological Reviews

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SUMMARY Immunity to pathogens is ensured through integration of early responses mediated by innate cells and late effector functions taking place after terminal differentiation of adaptive lymphocytes. In this context, innate lymphoid cells (ILCs) and adaptive T cells represent a clear example of how prototypical effector functions, including polarized expression of cytokines and/or cytotoxic activity, can occur with overlapping modalities but different timing. The ability of ILCs to provide early protection relies on their poised epigenetic state, which determines their propensity to quickly respond to cytokines and to activate specific patterns of signal-dependent transcription factors. Cytokines activating the Janus kinases (JAKs) and members of the signal transducer and activator of transcription (STAT) pathway are key regulators of lymphoid development and sustain the processes underlying T cell activation and differentiation. The role of the JAK/STAT pathway has been recently extended to several aspects of ILC biology. Here, we discuss how JAK/STAT signals affect ILC development and effector functions in the context of immune responses, highlighting the molecular mechanisms involved in regulation of gene expression, as well as, the potential of targeting the JAK/STAT pathway in inflammatory pathologies.

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“…D, Sorted total ILCs from controls or two STAT3 MT HIES patients were stimulated 20 min with media; IL-23 or IL-6 and pSTAT3 levels were measured by phospho-flow IL-7 is another cytokine critical for the generation, survival, proliferation, and maintenance of ILC3s in vitro and in vivo. [44][45][46][47][48][49] In this study, we…”

Section: Discussionmentioning

confidence: 99%