Dengue virus-specific CD8 T cell subsets are associated with specialized gene expression profiles and TCR repertoires
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA480690 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7511490.fastq.gz | Fastqsanger.gz | |||
| SRR7511500.fastq.gz | Fastqsanger.gz | |||
| SRR7511510.fastq.gz | Fastqsanger.gz | |||
| SRR7511491.fastq.gz | Fastqsanger.gz | |||
| SRR7511501.fastq.gz | Fastqsanger.gz |
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Project description:Accumulating evidence demonstrates that CD8 T cells contribute to protection from severe DENV disease and vaccine efficacy. Nevertheless, the molecular programs associated with DENV-specific CD8 T cell subsets have not been defined. Here, we studied the transcriptomic profiles of human DENV-specific CD8 T cells isolated after stimulation with DENV epitopes from donors that have been infected with DENV multiple times and should therefore associated with significant levels of adaptive immunity. DENV-specific CD8 T cells mainly consist of effector memory subsets, namely Tem and Temra which enact specific gene expression profiles upon stimulation with cognate antigens. DENV-specific CD8 T cell subsets in general, and Temra cells in particular, are fully activated and polyfunctional, yet associated with relatively narrow transcriptional responses and TCR repertoires. This study provides the first transcriptomic definition of DENV-specific activated human CD8 T cell subsets and defines a bench mark profile that vaccine-specific response could aim to reproduce.
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Project description:Clonal fate of helper T cells is governed by early costimulatory signals but may also depend on the mode of TCR interaction with peptide-MHC on APCs. We investigate TCR repertoires of eight effector/memory CD4+ T-cell subsets (Th1, Th2, nonclassical Th2 (Th2a), Th17, Th1-17, Tfh, Treg, Th22), revealing subset-specific physicochemical and recombinational features reproducible across donors. At a threshold of 3 reads per UMI, the number of obtained UMI-labeled cDNA molecules per repertoire per sample ranged from 5,300 to 303,500, and the number of CDR3 clonotype variants at the nucleotide level per repertoire per sample ranged from 1,200 to 83,200. Deep unbiased TCR profiling allowed us to assess the natural level of in vivo CD4+ subsets plasticity. We observed a major clonal exchange between Th17/Th22/Th2/Th2a and the high stability of Treg and Tfh subsets. The latter two subsets also show higher repertoire publicity across donors. Tfh repertoire features reflect those of mature antibodies and indicate stringent selection of highly antigen-specific, low cross-reactive TCRs. We conclude that functional subsets are marked with non-random universal for donors and specific features of passed selection. In future TCR sequencing applications, subset-specific profiling could provide better insights of normal and pathological states of adaptive immunity compared to the classical approach when TCR profiling is performed on bulk T cells or after rough division into CD4 and CD8-enriched populations.
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Project description:The avidity of the T-cell receptor (TCR) for antigenic peptides presented by the MHC (pMHC) on cells is an essential parameter for efficient T cell-mediated immunity. Yet, whether the TCR-ligand avidity can drive the clonal evolution of virus antigen-specific CD8 T cells, and how this process is determined in latent Cytomegalovirus (CMV)- against Epstein-Barr virus (EBV)-mediated infection remains largely unknown. Here, we quantified monomeric TCR-pMHC dissociation rates on CMV- and EBV-specific individual TCR-alpha-beta clonotypes and polyclonal CD8 T cell populations in healthy donors over a follow-up time of 15-18 years. Within CMV/pp65-specific T cell repertoires, a progressive contraction of clonotypes with high TCR-pMHC avidity and low CD8 binding dependency was observed, leading to an overall avidity decline during long-term antigen exposure. We identified a unique transcriptional signature preferentially expressed by high-avidity CMV/pp65-specific T cell clonotypes, including the inhibitory receptor LILRB1. Interestingly, T cell clonotypes of high-avidity showed higher LILRB1 expression than the low-avidity ones and LILRB1 blockade moderately increased T cell proliferation. Similar findings were made for CD8 T cell repertoires specific for the CMV/IE-1 epitope. There was a gradual in vivo loss of high-avidity T cells with time for both CMV specificities, corresponding to virus-specific CD8 T cells expressing enhanced LILRB1 levels. In sharp contrast, the EBV/BMFL1-specific T cell clonal composition and distribution, once established, displayed an exceptional stability, unrelated to TCR-pMHC binding avidity or LILRB1 expression. Together, these findings reveal an overall long-term avidity decline of CMV- but not EBV-specific T cell clonal repertoires, highlighting the differing role played by TCR-ligand avidity over the course of these two latent herpesvirus infections. Our data suggest that the inhibitor receptor LILRB1 potentially restricts the clonal expansion of high-avidity CMV-specific T cell clonotypes during latent infection. We propose that the mechanisms regulating the long-term outcome of CMV- and EBV-specific memory CD8 T cell clonotypes in humans are distinct.
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