Fetal-derived activated CD83+ γδ T cells expand in preterm infants with sepsis.
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE245131 | GEO | 2024/05/08
REPOSITORIES: GEO
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Project description:Fetal-derived activated CD83+ γδ T cells expand in preterm infants with sepsis.
| PRJNA1026987 | ENA
Project description:Human γδ T cells take a small but important part in the immune system. Human γδ T cells are usually categorized by the V gene of their T cell receptor (TCR) δ chain; most of which are Vδ1+ or Vδ2+. Naive γδ T cells are often found from neonates and cytotoxic γδ T cells (γδCTLs) are frequent in adults. However, phenotypes and the developmental programs of human γδ T cells are not fully clear. Here, by single-cell RNA sequencing (sc-RNAseq) of transcriptome and T cell receptor (sc-TCRseq) on γδ T cells from neonates and adults, we revealed human γδ T cells can be divided as naïve T cells, γδCTLs, and γδNKT cells which are featured by pro-Vδ1, Vδ1, and Vδ2 TCR repertoire, respectively. γδNKT cells can be further described as γδNKT-1, γδNKT-2, and γδNKT-17 cells.
2020-07-31 | GSE149356 | GEO
Project description:Bacterial sepsis is associated with high morbidity and mortality in preterm infants. However, diagnosis of sepsis and identification of the causative agent remains challenging. Our aim was to determine genome-wide expression profiles of very low birth weight (VLBW) infants with and without bacterial sepsis and assess differences.
2016-05-29 | E-MTAB-4785 | biostudies-arrayexpress
Project description:Neonates manifest a unique host response to sepsis even among other children. Preterm neonates may experience sepsis soon after birth or during often protracted birth hospitalizations as they attain physiologic maturity. We examined the transcriptome using genome-wide expression profiling on prospectively collected peripheral blood samples from infants evaluated for sepsis within 24 hours after clinical presentation. Simultaneous plasma samples were examined for alterations in inflammatory mediators. Group designation (sepsis or uninfected) was determined retrospectively based on clinical exam and laboratory results over the next 72 hours from the time of evaluation. Unsupervised analysis showed the major node of separation between groups was timing of sepsis episode relative to birth (early, <3 days or late, >3 days). Principal component analyses revealed significant differences between patients with early or late sepsis despite the presence of similar key immunologic pathway aberrations in both groups. Unique to neonates, the uninfected state and host response to sepsis is significantly affected by timing relative to birth. Future therapeutic approaches may need to be tailored to the timing of the infectious event based on post-natal age. We used human microarrays to detail the molecular profile of the events that occur following sepsis in hospitalized neonates Please note that 'uninfected chorio' represents babies who were not infected but had chorioamnionitis exposure
2015-07-06 | E-GEOD-69686 | biostudies-arrayexpress
Project description:Background: Neonatal infection and sepsis are common for preterm infants due to their immature immune system. Early diagnosis is important for effective treatment but few early markers of systemic and neuro-inflammatory responses in neonates are known. We hypothesized that systemic infection with Gram-positive Staphylococcus epidermidis (SE) induces acute changes to proteins in plasma and cerebrospinal fluid (CSF), potentially affecting the immature brain of preterm neonates. Methods: Using preterm pigs as model for preterm infants, plasma and CSF samples were collected up to 24 h after SE infection and investigated by untargeted mass spectrometry (MS)-based proteomics. Selected differential proteins were further studied in vitro assays. Results: The clinical signs of sepsis and neuroinflammation in SE-infected piglets were associated with changes in multiple CSF and plasma proteins. Eight plasma proteins, including APOA4, haptoglobin, MBL1, vWF, LBP and sCD14, were affected already 6 h after infection. Likewise, acute phase reactants, including complement components, showed a time-dependent activation pattern after infection. Feeding bovine colostrum reduced the sepsis-related change in clinical parameters as well as plasma proteins. Neuroinflammation-related neuropeptide Y (NPY), IL-18 and MMP-14 showed distinct changes in the CSF and several brain regions (prefrontal cortex, PVWM, hippocampus) 24 h after infection. These changes were verified in TLR2 agonist-challenged primary microglia cells, where exogenous NPY suppressed the inflammatory response. Conclusion: Systemic infection with Gram-positive SE induces inflammation with rapid proteome changes in plasma and CSF in preterm newborn pigs. The observed early markers of sepsis and neuroinflammation in preterm pigs may serve as novel biomarkers for sepsis in preterm infants.
2020-05-26 | PXD016013 | Pride
Project description:The mammalian gastrointestinal tract harbors thousands of bacterial species that include symbionts as well as potential pathogens. The immune responses that limit access of these bacteria to underlying tissue remain poorly defined. In this study, we used microarrays to uncover the transcriptional responses that occur in small intestinal γδ intraepithelial lymphocytes following bacterial challenge. γδ intraepithelial lymphocytes (γδ IEL) were isolated by flow cytometry from the small intestines of germ-free mice, or from age- and sex-matched conventionally-raised counterparts. We extracted RNAs from these purified γδ IEL for analysis on Affymetrix DNA microarrays. The mice were all >8 weeks in age, and each sample represents a pool of RNAs from 5-8 mice.
2011-04-06 | E-GEOD-28437 | biostudies-arrayexpress
Project description:Neonates manifest a unique host response to sepsis even among other children. Preterm neonates may experience sepsis soon after birth or during often protracted birth hospitalizations as they attain physiologic maturity. We examined the transcriptome using genome-wide expression profiling on prospectively collected peripheral blood samples from infants evaluated for sepsis within 24 hours after clinical presentation. Simultaneous plasma samples were examined for alterations in inflammatory mediators. Group designation (sepsis or uninfected) was determined retrospectively based on clinical exam and laboratory results over the next 72 hours from the time of evaluation. Unsupervised analysis showed the major node of separation between groups was timing of sepsis episode relative to birth (early, <3 days or late, >3 days). Principal component analyses revealed significant differences between patients with early or late sepsis despite the presence of similar key immunologic pathway aberrations in both groups. Unique to neonates, the uninfected state and host response to sepsis is significantly affected by timing relative to birth. Future therapeutic approaches may need to be tailored to the timing of the infectious event based on post-natal age.
2015-07-06 | GSE69686 | GEO
Project description:Influenza infection causes high rates of hospitalization and mortality in infants. γδ T cells are critical for immune responses against pathogens as regulators and effectors, especially in infants, and yet the roles of neonatal γδ T cells in influenza remain to be investigated. Here we report that γδ T cells were protective against mortality associated with neonatal influenza infection. Infection induced the accumulation and activation of γδ T cells, which transiently expressed IL-17a to enhance early IL-33 production by lung epithelial cells via STAT3 phosphorylation. Subsequently, this led to type 2 immune responses with elicited infiltration of ILC2s and Tregs resulting in increased amphiregulin secretion and tissue repair. Loss of γδ T cells did not alter viral clearance or IFN-γ production. Thus, our results identify a specific requirement for γδ T cells in influenza-infected neonates by initiating type 2 immune responses, mediating tissue homeostasis, and promoting lung integrity.
2018-06-20 | GSE99683 | GEO
Project description:RNA expression of unstimulated γδ-T cells,γδ-TCR-stimulated γδ-T cells, unstimulated αβ-TCR transduced γδ-T cells and αβ-TCR-stimulated αβ-TCR transduced γδ-T cells.
2023-09-07 | GSE216880 | GEO
Project description:Triple negative breast cancer (TNBC) lacks targeted therapy options. TNBC is enriched in breast cancer stem cells (BCSCs), which play a key role in metastasis, chemoresistance, relapse and mortality. γδ T cells hold great potential in immunotherapy against cancer, and might be an alternative to target TNBC. γδ T cells are commonly observed to infiltrate solid tumors and have an extensive repertoire of tumor sensing, recognizing stress-induced molecules and phosphoantigens (pAgs) on transformed cells. We show that patient derived triple negative BCSCs are efficiently recognized and killed by ex vivo expanded γδ T cells from healthy donors. Orthotopically xenografted BCSCs, however, were refractory to γδ T cell immunotherapy. Mechanistically, we unraveled concerted differentiation and immune escape: xenografted BCSCs lost stemness, expression of γδ T cell ligands, adhesion molecules and pAgs, thereby evading immune recognition by γδ T cells. Indeed, neither pro-migratory engineered γδ T cells, nor anti-PD 1 checkpoint blockade significantly prolonged overall survival of tumor-bearing mice. BCSC immune escape was independent of the immune pressure exerted by the γδ T cells, and could be pharmacologically reverted by Zoledronate or IFN-α treatment. These results pave the way for novel combinatorial immunotherapies for TNBC.
2023-07-20 | PXD039463 | Pride