Identification of IL-10 producing T cells in CSF and blood during treatment of subarachnoid neurocysticercosis
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ABSTRACT:
PROVIDER: PRJNA1084022 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR28231151.fastq.gz | Fastqsanger.gz | |||
| SRR28231152.fastq.gz | Fastqsanger.gz | |||
| SRR28231153.fastq.gz | Fastqsanger.gz | |||
| SRR28231154.fastq.gz | Fastqsanger.gz |
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Project description:Neurocysticercosis (NCC) is a parasitic infection that affects the central nervous system and is increasingly found in patients in non-endemic regions. Subarachnoid neurocysticercosis (SANCC) is the most severe form of this disease and is largely responsible for mortality associated with NCC. Inflammation is often an important factor in the treatment of SANCC as overactivity can lead to serious complications, but suppression induced by anti-inflammatory molecules – namely interleukin 10 (IL-10) – can lead to an increased time to cure. To better understand the local inflammatory milieu associated with SANCC, we performed single cell RNA sequencing to achieve an unbiased profile of immune cell populations in the cerebrospinal fluid (CSF), and we used flow cytometry to identify important producers of IL-10 in the CSF and blood. These analyses revealed a diverse combination of immune cell populations within the CSF including multiple myeloid and lymphoid populations. We identified three primary sources of IL-10 in CSF – natural regulatory T cells (nTregs), induced regulatory T cells (iTregs), and Th17 cells – with iTregs being the single largest contributor in this compartment. Our data also show that these populations – and the abundance of IL-10 producing CD4+ T cells as a whole – differed between CSF and blood. Interestingly, these IL-10 producing nTregs, iTregs, and Th17 cells persist in the CSF over the course of SANCC treatment, indicating that immunosuppression within the central nervous system is unaffected despite decreases in parasite antigen over time. Overall, this study deepens our understanding of the suppressive phenotype that deters SANCC treatment success and provides a comprehensive blueprint of the local and systemic immunology associated with this important disease process.
2024-10-30 | GSE260929 | GEO
Project description:IL-10 is a prototypical anti-inflammatory cytokine, which is fundamental to the maintenance of immune homeostasis, especially in the intestine. There is an assumption that cells producing IL-10 have an immunoregulatory function. However, here we report that IL-10-producing CD4+ T cells are phenotypically and functionally heterogeneous. By combining single cell transcriptome and functional analyses, we identified a subpopulation of IL-10-producing Foxp3Neg CD4+ T cells that displays regulatory activity unlike other IL-10-producing CD4+ T cells, which are unexpectedly pro-inflammatory. The combinatorial expression of co-inhibitory receptors is sufficient to discriminate IL-10-producing CD4+ T cells with regulatory function from others and to identify them across different tissues and disease models in mice and humans. These regulatory IL-10-producing Foxp3Neg CD4+ T cells have a unique transcriptional program, which goes beyond the regulation of IL-10 expression. Finally, we found that patients with Inflammatory Bowel Disease (IBD), demonstrate a deficiency in this specific regulatory T-cell subpopulation.
2018-11-07 | GSE121287 | GEO
Project description:IL-10 is a prototypical anti-inflammatory cytokine, which is fundamental to the maintenance of immune homeostasis, especially in the intestine. There is an assumption that cells producing IL-10 have an immunoregulatory function. However, here we report that IL-10-producing CD4+ T cells are phenotypically and functionally heterogeneous. By combining single cell transcriptome and functional analyses, we identified a subpopulation of IL-10-producing Foxp3Neg CD4+ T cells that displays regulatory activity unlike other IL-10-producing CD4+ T cells, which are unexpectedly pro-inflammatory. The combinatorial expression of co-inhibitory receptors is sufficient to discriminate IL-10-producing CD4+ T cells with regulatory function from others and to identify them across different tissues and disease models in mice and humans. These regulatory IL-10-producing Foxp3Neg CD4+ T cells have a unique transcriptional program, which goes beyond the regulation of IL-10 expression. Finally, we found that patients with Inflammatory Bowel Disease (IBD), demonstrate a deficiency in this specific regulatory T-cell subpopulation.
2018-11-07 | GSE121267 | GEO
Project description:IL-10 is a prototypical anti-inflammatory cytokine, which is fundamental to the maintenance of immune homeostasis, especially in the intestine. There is an assumption that cells producing IL-10 have an immunoregulatory function. However, here we report that IL-10-producing CD4+ T cells are phenotypically and functionally heterogeneous. By combining single cell transcriptome and functional analyses, we identified a subpopulation of IL-10-producing Foxp3Neg CD4+ T cells that displays regulatory activity unlike other IL-10-producing CD4+ T cells, which are unexpectedly pro-inflammatory. The combinatorial expression of co-inhibitory receptors is sufficient to discriminate IL-10-producing CD4+ T cells with regulatory function from others and to identify them across different tissues and disease models in mice and humans. These regulatory IL-10-producing Foxp3Neg CD4+ T cells have a unique transcriptional program, which goes beyond the regulation of IL-10 expression. Finally, we found that patients with Inflammatory Bowel Disease (IBD), demonstrate a deficiency in this specific regulatory T-cell subpopulation.
2018-11-07 | GSE121284 | GEO
Project description:IL-10 is a prototypical anti-inflammatory cytokine, which is fundamental to the maintenance of immune homeostasis, especially in the intestine. There is an assumption that cells producing IL-10 have an immunoregulatory function. However, here we report that IL-10-producing CD4+ T cells are phenotypically and functionally heterogeneous. By combining single cell transcriptome and functional analyses, we identified a subpopulation of IL-10-producing Foxp3Neg CD4+ T cells that displays regulatory activity unlike other IL-10-producing CD4+ T cells, which are unexpectedly pro-inflammatory. The combinatorial expression of co-inhibitory receptors is sufficient to discriminate IL-10-producing CD4+ T cells with regulatory function from others and to identify them across different tissues and disease models in mice and humans. These regulatory IL-10-producing Foxp3Neg CD4+ T cells have a unique transcriptional program, which goes beyond the regulation of IL-10 expression. Finally, we found that patients with Inflammatory Bowel Disease (IBD), demonstrate a deficiency in this specific regulatory T-cell subpopulation.
2018-11-07 | GSE121386 | GEO
Project description:During chronic viral infection, the inflammatory function of CD4 T cells becomes gradually attenuated. Concurrently, Th1 cells progressively acquire the capacity to secrete the cytokine IL-10, a potent suppressor of antiviral T cell responses. To determine the transcriptional changes that underlie this T cell adaption process, we applied a single-cell RNA-sequencing approach and assessed the heterogeneity of IL-10-expressing CD4 T cells during chronic infection. Unexpectedly, our analyses revealed an IL-10-producing population with a robust Tfh-signature. Using IL-10 and IL-21 double-reporter mice, we further demonstrate that IL-10+IL-21+co-producing Tfh cells arise predominantly during chronic but not acute LCMV infection. Importantly, depletion of IL-10+IL-21+co-producing CD4 T cells or deletion of Il10 specifically in Tfh cells resulted in impaired humoral immunity and viral control. Mechanistically, B cell-intrinsic IL-10 signaling was required for sustaining germinal center reactions. Lastly, we demonstrate that IL-27 and type I IFNs differentially regulate the formation of this protective IL-10-producing Tfh subset. Thus, our findings elucidate a critical role for Tfh-derived IL-10 in promoting humoral immunity during persistent viral infection.
2018-10-29 | GSE111026 | GEO
Project description:Transcriptional profiling of human peripheral B cell subsets sorted by flow cytometry based on the secretion of IL-10 in response to CpG2006 stimulation. Goal was to identify molecular markers to distinguish IL-10-producing B cells form non-IL-10-producing B cells.
2013-03-04 | GSE35002 | GEO
Project description:Background information: Antibody responses to most infectious and food protein antigens depend on help to B cells from specialised T follicular helper (Tfh) cells. A subset of Foxp3+ regulatory T cells (Tregs) has been described in mice, with a prominent role in repressing germinal center reactions that are critical for memory B cell formation and long-lived antibody responses. These specialised Tregs co-opt the Bcl-6-dependent Tfh differentiation pathway in order to access the B cell-rich follicles and have therefore been designated as T follicular regulatory (Tfr) cells. Preliminary results: We identified a unique Bcl-6-expressing follicular regulatory T cell in human secondary lymphoid tissue, designated hereafter as Tfr2 cells, that lacks Foxp3 expression and the thymic-imprinted Foxp3 methylation pattern, but shares expression of key Treg molecules. Interestingly, 25% of these cells are the predominant source of T cell-derived IL-10 in human tonsil, an important cytokine with immunomodulatory properties. Aims of this study: We performed transcriptional profiling using affymetrix microarrays to interrogate wether IL-10 producing vs non producing human Tfr2 cells were fundamentally different subsets. 2 cell types (IL-10+ vs IL10- TFR2 cell subsets) obtained from 3 different tonsil donors (biological replicates)
2016-04-05 | E-GEOD-79887 | biostudies-arrayexpress
Project description:IL-2 is one of the first cytokine discovered but its complex roles in T cell effector functions has shadowed its function in B cell responses. B cells transiently expressed IL-2 receptor upon activation but it is unclear whether all mature B cell subsets have an equal dependence upon IL-2 and how IL-2 dictates B cell fate. Using our newly generated B-cell-specific Il2rb conditional knockout (KO) model of mice lacking IL2RB signaling in mature B cells, our objectives were to: (1) transcriptionally characterize IL-10-producing B cells induced by IL-2 ; (2) explore a potential commitment of these IL-10-secreting B cells ; (3) decipher IL-2 mechanisms of action on B cells by identifiying signal transducers and/or transcriptional players mobilised in immunoregulatory polarization program iniated by IL-2 signaling. We found that IL-2 acts intrinsically on B cells to promote Maf and Il10 expression and engage B cells toward immunoregulatory profile. In parallele, we found that IL-2 promotes plasma cell reprogramming on IL-10-producing B cells.
2025-10-30 | GSE280677 | GEO
Project description:The mechanisms in regulating the development of IL-10 producing B cells are largely unknown. To clarify which transcription factor is critical for regulation of IL-10 producing B cells, we compared the gene expression profile of IL-10 positive B cells and IL-10 negative B cells. Transcriptional repressor Prdm1/Blimp1 is known to play a key role in controlling B ells differentiation. We show a dual role for Blimp-1 in IL-10 expression in IL-10 producing B cells and plasmablasts.
2019-09-11 | GSE129260 | GEO