KLRG1+ Memory CD8 T cells Combine Properties of Short-lived Effectors and Long-lived Memory
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA640616 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12054802_1.fastq.gz | Fastqsanger.gz | |||
| SRR12054802_2.fastq.gz | Fastqsanger.gz | |||
| SRR12054803_1.fastq.gz | Fastqsanger.gz | |||
| SRR12054803_2.fastq.gz | Fastqsanger.gz | |||
| SRR12054804_1.fastq.gz | Fastqsanger.gz |
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Project description:CD8 effector T cells with a CD127hi KLRG1- phenotype are considered precursors to the long-lived memory pool, while KLRG1+ CD127low cells are viewed as short-lived effectors. Nevertheless, we and others have shown that a KLRG1+ CD127low population persists into the memory phase and that these T cells (termed long-lived effector cells or LLEC) display robust protective function during acute re-challenge with bacteria or viruses. Whether these T cells represent a true memory population or are instead a remnant effector cell population that failed to undergo initial contraction has remained unclear. Here, we show that LLEC from mice express a distinct phenotypic and transcriptional signature that shares characteristics of both early effectors and long-lived memory cells. Furthermore, we find that LLEC are exclusively derived from day 12 KLRG1+ effector cells. Our work challenges the concept that the KLRG1+ CD127low population is dominated by short-lived cells and shows that KLRG1 downregulation is not a prerequisite to become a long-lived protective memory T cell.
2020-08-26 | GSE152841 | GEO
Project description:The goal of this study is to characterize the transcriptional profile of three memory CD8 T cell subsets: IL-7Rα+KLRG1- (memory precursors, MP), IL-7Rα+KLRG1+ (KLRG1+ MP) and IL-7Rα-KLRG1+ (terminal effectors, TE).
2022-12-12 | GSE218777 | GEO
Project description:CD8 effector T cells with a CD127hi KLRG1- phenotype are considered precursors to the long-lived memory pool, whereas KLRG1+CD127low cells are viewed as short-lived effectors. Nevertheless, we and others have shown that a KLRG1+CD127low population persists into the memory phase and that these T cells (termed long-lived effector cells [LLEC]) display robust protective function during acute rechallenge with bacteria or viruses. Whether these T cells represent a true memory population or are instead a remnant effector cell population that failed to undergo initial contraction has remained unclear. In this study, we show that LLEC from mice express a distinct phenotypic and transcriptional signature that shares characteristics of both early effectors and long-lived memory cells. We also find that in contrast to KLRG1+ effector cells, LLEC undergo homeostatic proliferation and are not critically dependent on IL-15 for their maintenance. Furthermore, we find that LLEC are predominantly derived from KLRG1+ effector cells when isolated at day 12 of the response. Our work challenges the concept that the KLRG1+CD127low population is dominated by short-lived cells and shows that KLRG1 downregulation is not a prerequisite to become a long-lived protective memory T cell.
| S-EPMC7415731 | biostudies-literature
Project description:RNA-sequencing of three murine memory CD8 T cell subsets: IL-7Rα+KLRG1- , IL-7Rα+KLRG1+, and IL-7Rα-KLRG1+
| PRJNA905436 | ENA
Project description:During acute viral infections in mice, IL-7Rα and KLRG1 together are used to distinguish the short-lived effector cells (SLEC; IL-7RαloKLRGhi) from the precursors of persisting memory cells (MPEC; IL-7RαhiKLRG1lo). We here show that these markers can be used to define distinct subsets in the circulation and lymph nodes during the acute phase and in ‘steady state’ in humans. In contrast to the T cells in the circulation, T cells derived from lymph nodes hardly contain any KLRG1-expressing cells. The four populations defined by IL-7Rα and KLRG1 differ markedly in transcription factor, granzyme and chemokine receptor expression. When studying renal transplant recipients experiencing a primary hCMV and EBV infection, we also found that after viral control, during latency, Ki-67-negative SLEC can be found in the peripheral blood in considerable numbers. Thus, combined analyses of IL-7Rα and KLRG1 expression on human herpes virus-specific CD8+ T cells can be used to separate functionally distinct subsets in humans. As a non-cycling IL-7RαloKLRG1hi population is abundant in healthy humans, we conclude that this combination of markers not only defines short-lived effector cells during the acute response but also stable effector cells that are formed and remain present during latent herpes infections.
2019-02-01 | GSE113098 | GEO
Project description:The events controlling transition of T cells from effector to memory remain poorly understood. Herein, we defined two types of effectors on the basis of cell division, expression of activation markers and production of effector cytokines and investigated their potential for memory generation. The results indicated that the moderately activated early effectors readily transit to memory while highly activated late effectors develop minimal memory. Boosting with antigen-free adjuvant, however, rescues the late effectors from cell death and sustains both survival and cytokine responses through toll-like receptor function. Also, the genome-wide microarray analysis among early and late effectors pointed to a set og defined as well as less known genes that may play a role in transition to memory. CFSE-labeled DO11.10 CD4 naïve T cells were transferred into Balb/c mice and the hosts were immunized with OVA peptide in CFA. Within 3 days, the lymph node cells were harvested and each effector division (from division 2 to 8) was sorted based on CFSE dilution and then they were either transferred into naive hosts to generate memory cells or their RNAs were extracted to perform genome-wide microarray analysis. To correlate gene expression with memory potential, division 4 (D4), which readily transit to memory, and divisions 3 (D3), 6 (D6) and 8 (D8), which display reduced potential for memory transition, were included. The data were derived from 3 independent experiments (3 samples per division, 12 samples total).
2011-01-01 | E-GEOD-25141 | biostudies-arrayexpress
Project description:The events controlling transition of T cells from effector to memory remain poorly understood. Herein, we defined two types of effectors on the basis of cell division, expression of activation markers and production of effector cytokines and investigated their potential for memory generation. The results indicated that the moderately activated early effectors readily transit to memory while highly activated late effectors develop minimal memory. Boosting with antigen-free adjuvant, however, rescues the late effectors from cell death and sustains both survival and cytokine responses through toll-like receptor function. Also, the genome-wide microarray analysis among early and late effectors pointed to a set og defined as well as less known genes that may play a role in transition to memory.
2011-01-01 | GSE25141 | GEO
Project description:KLRG1+ Effector CD8+ T Cells Lose KLRG1, Differentiate Into All Memory T Cell Lineages, and Convey Enhanced Protective Immunity
| PRJNA434329 | ENA
Project description:The involvement of γδ TCR-bearing lymphocytes in immunological memory has gained increasing interest due to their functional duality between adaptive and innate immunity. γδ T effector memory (TEM) and central memory (TCM) subsets have been identified, but their respective roles in memory responses are poorly understood. In the present study, we used subsequent mouse cytomegalovirus (MCMV) infections of αβ T cell deficient mice in order to analyze the memory potential of γδ T cells. As for CMV-specific αβ T cells, MCMV induced the accumulation of cytolytic, KLRG1+CX3CR1+ γδ TEM that principally localized in infected organ vasculature. Typifying T cell memory, γδ T cell expansion in organs and blood was higher and more efficient after secondary viral challenge than after primary infection. Viral control upon MCMV reinfection was prevented when masking γδ T-cell receptor, and was associated with a preferential amplification of private and unfocused TCR δ chain repertoire composed of a combination of clonotypes expanded post-primary infection and, more unexpectedly, of novel expanded clonotypes. Finally, long-term-primed γδ TCM cells, but not γδ TEM cells, protected T cell-deficient hosts against MCMV-induced death upon adoptive transfer, probably through their ability to survive and to generate TEM in the recipient host. This better survival potential of TCM cells was confirmed by a detailed scRNASeq analysis of these two γδ T cell subsets which also revealed their similarity to classically adaptive αβ CD8 T cells. Overall, our study uncovered memory properties of long-lived TCM γδ T cells that confer protection in a chronic infection, highlighting the interest of this T cell subset in vaccination approaches.
2024-07-25 | GSE269394 | GEO
Project description:Memory B cells represent one of the pillar of humoral protection and are found in the circulation and secondary lymphoid organs several decades after initial pathogen or vaccine encounter. The exact cellular and biological mechanisms allowing long-term survival of quiescent cells in such a fluctuating microenvironment remain poorly understood. Assessing the true longevity of human memory B cells against common pathogens is, in most settings, hindered by the possibility for any given individual to re-encounter them during his lifetime. Smallpox, officially declared eradicated in 1980 (Fenner WHO 1988), represents one notable exception. Alongside smallpox eradication, anti-smallpox vaccination, based on the live Vaccinia virus, was progressively discontinued during the 1970s. As such, any detectable anti-vaccinia memory B cell in an individual post 2010 would likely have been generated more than 40 years ago, without any re-stimulation with the immunizing antigen during that timeframe. Anti-vaccinia antibodies serum titers remain stable in human for more than 80 years after first vaccination (Amanna NEJM 2007, PMID: 17989383), with several identified immunodominant epitopes including the envelope glycoprotein B5R (Lantto J Virol 2011, PMID: 21147924). Anti-vaccinia memory B cells have similarly been followed longitudinally in the blood for up to 65 years post vaccination (Amanna NEJM 2007, PMID: 17989383 ; Crotty JI 2003, PMID : 14607890) and, following a contraction phase taking place in the first couple of years after immunization, reach a remarkably stable plateau that last for decades at around 0.1% of total circulating IgG+ memory B cells. Functional analysis of such long-lived memory B cells, however, is still lacking. As a proxy to study long-lived memory B cells, IgG+ switched memory B cells specific for the immunodominant Vaccinia antigen B5R (B5R+ IgG+ memory B cells) were sorted and analyzed by scRNAseq from the spleen of six organ donors, collected between 2015 and 2018. For all donors, B5R+ IgG+ memory B cells were sorted alongside total IgG+ memory B cells (live IgD-CD27+IgG+CD20+CD3-CD14-CD16-) and naïve B cells (live IgD+CD27-CD38-CD24-CD20+CD3-CD14-CD16-). Single-cell mRNA sequencing was performed according to an adapted version of the SORT-seq protocol (Muraro et al., 2016, PMID: 27693023), with cDNA libraries generation, sequencing and reads alignment performed at Single Cell Discoveries (Utrecht, Netherlands).
2022-09-19 | E-MTAB-11626 | biostudies-arrayexpress