Analyses of ILC3s from the mesenteric lymph nodes (LN)
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE76201 | GEO | 2016/02/15
SECONDARY ACCESSION(S): PRJNA306619
REPOSITORIES: GEO
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Project description:Analyses of ILC3s in Rorc floxed control and Id2iÎ?RORγt mice following daily treatments of tamoxifen for two weeks. Cells were sort purified as lineage negative, CD127+ CD90.2+ CCR6+ ST2- CCR6+ ILCs were sorted from the mesenteric LN of Rorc floxed control and Id2iÎ?RORγt mice following daily treatments of tamoxifen for two weeks.
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2015-05-21 | E-GEOD-67076 | biostudies-arrayexpress
Project description:Human ILCs are classically categorized into five subsets; cytotoxic CD127-CD94+ NK cells and non-cytotoxic CD127+CD94-, ILC1s, ILC2s, ILC3s and LTi cells. Here, we identify a novel subset within the CD127+ ILC population, characterized by the expression of the cytotoxic marker CD94. These CD94+ ILCs strongly resemble conventional ILC3s in terms of phenotype, transcriptome and cytokine production, but are highly cytotoxic. IL-15 was unable to induce differentiation of CD94+ ILCs towards mature NK cells. Instead, CD94+ ILCs retained RORγt, CD127 and CD200R expression and produced IL-22 in response to IL-15. Culturing non-cytotoxic CD127+ ILC1s or ILC3s with IL-12 induced upregulation of CD94 and cytotoxic activity, effects that were not observed with IL-15 stimulation. Thus, human helper ILCs can acquire a cytotoxic program without differentiating into NK cells.
2020-09-14 | GSE147231 | GEO
Project description:We unexpectedly identify one unique subset of group 3 innate lymphoid cells (ILC3s) that co-expresses Zbtb46, a transcription factor that specifies conventional dendritic cells (cDCs). Zbtb46 is robustly expressed by CCR6+ lymphoid tissue inducer (LTi)-like ILC3s that are developmentally and phenotypically distinct from cDCs. To determine the function of Zbtb46 in ILC3s, we performed RNA sequencing on CCR6+ ILC3s sorted from the large intestine of Zbtb46 f/f and Rorc Cre Zbtb46 f/f mice at steady state.
2022-05-02 | GSE181865 | GEO
Project description:ILC3s from the spleen (SP) and small intestine (SI) have been shown to be phenotypically and functional different. Intestinal factors are likely to regulate transcriptional profiles and thereby function of ILC3s. The goal of this study is to analyze if SI ILC3s acquire a SP-similar transcriptional profile after in vitro culture. Therefore transcriptional profiles of cultured SI ILC3s were compared to freshly isolated ILC3s of the murine SP and the SI by RNA seq technology. Cell suspension were generated from both organs and ILC3s (CD117+, Thy1.2+, KLRG1-, lin- (CD3, CD8, CD11b, CD11c, CD19, B220, Gr-1, TCRβ, TCRγδ, TER-119, NK1.1)) were sort purified. SI ILC3 were cultured for 7 days in vitro with IL-2, IL-7 and SCF. RNA was isolated and RNA sequencing was done using Ilumina Hiseq 2500 system and NuGEN Ovation RNA Seq System V2, with biological replicates. We show that intestinal ILC3 acquire a splenic-similar transcriptional profile after in vitro culture.
2020-03-17 | GSE114750 | GEO
Project description:GATA3 is indispensable for the development of all IL-7Rα-expressing innate lymphoid cells (ILCs) and maintenance of type 1 ILCs (ILC1s) and type 2 ILCs (ILC2s). However, the importance of low GATA3 expression in type 3 ILCs (ILC3s) is still elusive. Here, we report that GATA3 regulates homeostasis of ILC3s by controlling IL-7Rα expression. In addition, GATA3 is critical for the development of NKp46+ ILC3 subset partially through regulating the balance between T-bet and RORγt. Genome-wide analyses indicate that while GATA3 positively regulates CCR6+ and NKp46+ ILC3 subset-specific genes in respective lineages, it negatively regulates CCR6+ ILC3-specific genes in NKp46+ ILC3s. Furthermore, GATA3 regulates IL-22 production in both CCR6+ and NKp46+ ILC3s. Thus, low GATA3 expression is critical for the development and function of ILC3 subsets. To identify GATA3 regulated genes in total ILC3s with RNA-Seq; To identify unique genes expressed by CCR6+ ILC3 or NKp46+ ILC3 and GATA3 regulated genes within these two ILC3 subsets with RNA-Seq; To identify GATA3 direct binding sites in ILC3s, ILC2s and Th2 cells with ChIP-Seq.
2015-11-23 | E-GEOD-71198 | biostudies-arrayexpress
Project description:In order to determine the dependency of mature tissue-resident ILCs on combinations of synergistic and antagonising Transcription Factors (TFs), we generated mice with conditional deletions of RORc, RORa and Tbx21 driven from the Id2 allele, utilizing a tamoxifen inducible Cre-recombinase in combination with a tdRFP allele to report Cre-excision (Id2creERT2 x ROSAtdRFP). RFP+ small intestinal ILCs were sorted from the lamina propria digests (gated as CD45+, Lineage negative, CD90+ CD127+, tdRFP+ - see manuscript for full methodological details), from control mice or mice containing loxP flanked alleles for RORc, RORc and RORa or RORc and Tbx21. Four samples of sort-purified ILCs were then subjected to 10X single cell sequencing; - Id2creERT2 - Id2idRORc - Id2idRORc/RORa - Id2idRORc/Tbx21
2021-09-23 | E-MTAB-9795 | biostudies-arrayexpress
Project description:Splenic and intestinal NCR- ILC3s have been shown to be phenotypically and functional different. The goal of this study is to compare transcriptional profiles of NCR- ILC3s isolated of the murine spleen (SP) and the small intestine (SI) by RNA seq technology. Cell suspension were generated from both organs and NCR- ILC3s (CD117+, Thy1.2+, eYFP+, lin- (CD3, CD8, CD11b, CD11c, CD19, B220, Gr-1, TCRβ, TCRγδ, TER-119, NK1.1, NKp46)) were sort purified. RNA was isolated and RNA sequencing was done using Ilumina Hiseq 2500 system and NuGEN Ovation RNA Seq System V2, with biological triplicates. We provide the first comparison of transcriptional profiles of intestinal and splenic NCR- ILC3s.
2020-03-17 | GSE114749 | GEO
Project description:Background: Alternaria exposure is associated with severe asthma in humans. Alternaria exposure in mice potently activates group 2 innate lymphoid cells (ILC2s) via the IL-33/ST2 axis and causes ILC2s to robustly secrete type 2 cytokines. Objective: Our aim was to determine whether conventionally used ILC2 markers, ST2 (IL-33R) and CD127 (IL-7Ra), were sufficient to identify all Th2-cytokine producing ILCs after Alternaria exposure. Methods: Mice received intranasal Alternaria for three days prior to analysis. Lung ILCs were identified by flow cytometry as CD45+Lineage−Thy1.2+ lymphocyte-sized cells, divided into four subsets based on ST2 and CD127 expression, and stained for intracellular cytokines and transcription factors. Sort-purified ILC subpopulations were also analyzed by RNA sequencing and qPCR. Results: Alternaria exposure led to accumulation of all ILC populations regardless of ST2 or CD127 expression. Nearly half of the GATA-3+, IL-5+, and IL-13+ ILCs were “unconventional” as they were either single or double negative for ST2/CD127. Further, these populations upregulated CD25, KLRG1, and ICOS after Alternaria challenge. Some activated unconventional IL-5+ ILC2s also produced IFNγ and IL-17A. In addition to shared ILC2 transcripts (Gata3, Il5, Il13) in all populations, RNA-seq further identified novel transcripts enriched in each subset. Finally, transcripts from all populations that correlated best with IL-5 and IL-13 production included Tnfrsf18, Ffar2, and Pde4b. Conclusions: Unconventional ST2- and CD127-negative mouse lung ILC2 populations are induced by Alternaria. Thus, commonly used lung ILC2 identification methods based on ST2 and CD127 do not accurately account for the total ILC2 burden and may exclude nearly half of these cells.
2019-08-22 | GSE136156 | GEO