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Subunit vaccine elicited lung TRM cells use fibroblast IL-17R signaling to provide serotype independent immunity against hypervirulent K. pneumoniae

ABSTRACT: Subunit vaccine elicited lung TRM cells use fibroblast IL-17R signaling to provide serotype independent immunity against hypervirulent K. pneumoniae

PROVIDER: PRJNA661089 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12576418_1.fastq.gz	Fastqsanger.gz
	SRR12576418_2.fastq.gz	Fastqsanger.gz
	SRR12576419_1.fastq.gz	Fastqsanger.gz
	SRR12576419_2.fastq.gz	Fastqsanger.gz
	SRR12576420_1.fastq.gz	Fastqsanger.gz

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Subunit vaccine elicited lung TRM cells use fibroblast IL-17R signaling to provide serotype independent immunity against hypervirulent K. pneumoniae

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Vaccine driven lung TRM cells provide immunity against Klebsiella via fibroblast IL-17R signaling [scRNA-Seq]

Project description:Vaccine driven lung TRM cells provide immunity against Klebsiella via fibroblast IL-17R signaling [scRNA-Seq]

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Vaccine-driven lung TRM cells provide immunity against <i>Klebsiella</i> via fibroblast IL-17R signaling.

Project description:Tissue-resident memory (TRM) cells are thought to play a role in lung mucosal immunity to pathogens, but strategies to elicit TRM by mucosal vaccines have not yet been fully realized. Here, we formulated a vaccine composed of outer membrane protein (Omp) X from Klebsiella pneumoniae and LTA1 adjuvant that was administered by the intrapulmonary route. This vaccine elicited both TH1 and TH17 cells that shared transcriptional features with cells elicited by heat-killed K. pneumoniae. Antibody responses were required to prevent bacterial dissemination but dispensable for lung-specific immunity. In contrast, lung immunity required CD4+ T cells, STAT3 expression, and IL-17R signaling in fibroblasts. Lung-specific CD4+ T cells from OmpX+LTA1–immunized mice were observed homing to the lung and could mediate protection against infection in an adoptive transfer model. Vaccine-elicited TH17 cells showed reduced plasticity and were resistant to the immunosuppressant FK506 compared with TH1 cells, and TH17 cells conferred protection under conditions of transplant immunosuppression. These data demonstrate a promising vaccine strategy that elicits lung TRM cells and promotes serotype-independent immunity to K. pneumoniae.

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Vaccine driven lung TRM cells provide immunity against Klebsiella via fibroblast IL-17R signaling

Project description:Subunit vaccine elicits lung tissue resident memmory CD4+ T-cells and confers lung protection against heterologous strain

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Vaccine driven lung TRM cells provide immunity against Klebsiella via fibroblast IL-17R signaling [scRNA-Seq]

Project description:Subunit vaccine elicits lung tissue resident memmory CD4+ T-cells and confers lung protection against heterologous strain

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Intestinal IL-17R signaling controls liver inflammation by constraining microbiome-induced TLR9 signaling and IL-18 production

Project description:IL-17 and IL-17R signaling in the intestinal epithelium regulate the intestinal microbiome. Given the reported links between intestinal dysbiosis, bacterial translocation, and liver disease, we hypothesized that intestinal IL-17R signaling plays a critical role in mitigating hepatic inflammation. To test this, we studied intestinal epithelial-specific IL-17RA deficient mice in a model of concanavalin A hepatitis. Absence of enteric IL-17RA signaling exacerbated hepatitis and hepatocyte cell death. These mice exhibited commensal dysbiosis, increased intestinal and liver Il18, and increased liver translocation of bacterial products, specifically CpG DNA. Mechanistically, CpG DNA induced hepatic IL-18, increasing IFNγ and FasL in hepatic T-cells to drive inflammation. Thus, intestinal IL-17R regulates translocation of TLR9 ligands and constrains susceptibility to hepatitis. These data connect enteric Th17 signaling and the microbiome in hepatitis, with broader implications on the effects of impaired intestinal immunity and subsequent release of microbial products seen in other extra-intestinal pathologies.

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Hobit identifies TRM precursors that are regulated by Eomes

Project description:Tissue-resident memory CD8+ T cells (TRM) constitute a non-circulating memory T cell subset that provides early protection against re-infection. However, how TRM arise from antigen-triggered T cells has remained unclear. Exploiting the TRM-restricted expression of Hobit, we developed TRM reporter/deleter mice to study TRM differentiation. We found that Hobit was upregulated in a subset of LCMV-specific T cells located within peripheral tissues during the effector phase of the immune response. These Hobit+ effector T cells were identified as TRM precursors, given that their depletion substantially decreased TRM development, but not the formation of circulating memory T cells. Adoptive transfer experiments of Hobit+ effector T cells corroborated their biased contribution to the TRM lineage. Transcriptional profiling of Hobit+ effector T cells underlined the early establishment of TRM properties including downregulation of tissue exit receptors and upregulation of TRM-associated molecules. Importantly, we identified Eomes as a key factor instructing the early bifurcation of circulating and resident lineages. These findings establish that commitment of TRM occurs early in antigen-driven T cell differentiation and reveal the molecular mechanisms underlying this differentiation pathway.

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Project description:The ability to detect and isolate human CD8 TSP (Side population), NaÃ¯ve, Effector memory (EM), Central memory (CM) cells allowed us to compare the global gene expression profiles of these cells. Human TSP cells comprise of distinct gene expression profile specifically enriched for genes overexpressed in TRM cells. RNA samples from CD8 TSP (Side population), NaÃ¯ve, Effector memory (EM), Central memory (CM) cells were amplified, labeled, and hybridized on the Affymetrix Human Genome U133 Plus 2.0 microarray chips. The data were analyzed with GeneSpring GX 12.5 (Agilent Technologies)

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Vaccine-elicited IL-1R signaling results in Th17 TRM-mediated immunity.

Project description:Lung tissue resident memory (TRM) cells are thought to play crucial roles in lung host defense. We have recently shown that immunization with the adjuvant LTA1 (derived from the A1 domain of E. coli heat labile toxin) admixed with OmpX from K. pneumoniae can elicit antigen specific lung Th17 TRM cells that provide serotype independent immunity to members of the Enterobacteriaceae family. However, the upstream requirements to generate these cells are unclear. Single-cell RNA-seq showed that vaccine-elicited Th17 TRM cells expressed high levels of IL-1R1, suggesting that IL-1 family members may be critical to generate these cells. Using a combination of genetic and antibody neutralization approaches, we show that Th17 TRM cells can be generated independent of caspase-1 but are compromised when IL-1α is neutralized. Moreover IL-1α could serve as a molecular adjuvant to generate lung Th17 TRM cells independent of LTA1. Taken together, these data suggest that IL-1α plays a major role in vaccine-mediated lung Th17 TRM generation.

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