Ontology highlight
ABSTRACT:
PROVIDER: PRJNA681115 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13164983_1.fastq.gz | Fastqsanger.gz | |||
| SRR13164983_2.fastq.gz | Fastqsanger.gz | |||
| SRR13164984_1.fastq.gz | Fastqsanger.gz | |||
| SRR13164984_2.fastq.gz | Fastqsanger.gz | |||
| SRR13164985_1.fastq.gz | Fastqsanger.gz |
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Project description:CD8+ T cells contribute to the antiviral response in simian immunodeficiency virus (SIV) infection in nonhuman primates subsequent to recognition of viral epitopes via the T cell receptor (TCR). In previous studies, we examined the TCR repertoire of CD8+ T cells specific for a single SIV immunodominant epitope, Gag-CM9 (CTPYDINQM), throughout SIV infection. We identified tissue specific TCR sequences and TCRs shared by multiple anatomical sites. We now sought to evaluate if the tissue localization or TCR sequence of a CM9 specific CD8+ T cell corresponds with a transcriptional phenotype. CM9 specific CD8+ T cells were sorted from blood, lymph nodes, spleen, and liver from SIV infected rhesus macaques. The cells were processed through a single cell sequencing protocol, creating a TCR amplified library and an RNA gene expression library for each cell. Gene Set Enrichment Analysis (GSEA) revealed no distinct transcriptional profiles for CM9 specific CD8+ T cells between different anatomical sites and between cells with shared or tissue specific TCRs. Similarly, no clear transcriptional profiles were associated with public clonotypes. CM9 specific CD8+ T cells from posttreatment controllers did exhibit enrichment of select pathways compared to non-controllers. These data suggest that, while antigen specific CD8+ T cells from non-controllers exhibit largely similar transcriptional profiles, altered transcription in antigen specific CD8+ T cells from post-treatment controllers may associate with viral control.
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Project description:This study examines the extent to which memory CD4+ T cells share immunosurveillance strategies with CD8+ resident memory T cells (TRM). After acute viral infection, memory CD4+ T cells predominantly utilized residence to survey nonlymphoid tissues, albeit not as stringently as observed for CD8+ T cells. In contrast, memory CD4+ T cells were more likely to be resident within lymphoid organs than CD8+ T cells. Migration properties of memory-phenotype CD4+ T cells in non-SPF parabionts were similar, generalizing these results to diverse infections and conditions. CD4+ and CD8+ TRM shared overlapping transcriptional signatures and location-specific features, such as granzyme B expression in the small intestine, revealing tissue-specific and migration property-specific, in addition to lineage-specific, differentiation programs. Functionally, mucosal CD4+ TRM reactivation locally triggered both chemokine expression and broad immune cell activation. Thus, residence provides a dominant mechanism for regionalizing CD4+ T cell immunity, and location enforces shared transcriptional, phenotypic, and functional properties with CD8+ T cells.
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Project description:CD8+ memory T cells are critical components of protective immunity to intracellular pathogens and tumors. While many memory CD8+ T cells recirculate throughout the body, others remain lodged in tissues and guard common sites of pathogen entry. Contributions of the specific tissue environment to tissue-resident memory T cell (Trm) differentiation and homeostasis have been implicated but are not well understood. Here, we define the diversity of gene expression and genome accessibility by mouse CD8+ Trm populations in distinct organs and identify molecules critical for Trm generated in response to acute viral infection. We find that CD8+ TRM across different tissues possess both shared and tissue-specific transcriptional and epigenetic signatures. Notably, Trm in the intestine and salivary gland express TGFb-induced genes and are maintained by ongoing TGFb signaling while those in the fat, kidney, and liver are not. By constructing transcriptional-regulatory networks for each Trm population, we identify the repressor Hic1 as a critical regulator of Trm differentiation, particularly for Trm of the small intestine. This study provides a framework for understanding how Trm adapt to distinct tissue environments and identifies tissue-specific transcriptional regulators that mediate these adaptations, informing strategies to enhance protective memory responses at the sites most vulnerable to infection.
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Project description:CD8+ memory T cells are critical components of protective immunity to intracellular pathogens and tumors. While many memory CD8+ T cells recirculate throughout the body, others remain lodged in tissues and guard common sites of pathogen entry. Contributions of the specific tissue environment to tissue-resident memory T cell (Trm) differentiation and homeostasis have been implicated but are not well understood. Here, we define the diversity of gene expression and genome accessibility by mouse CD8+ Trm populations in distinct organs and identify molecules critical for Trm generated in response to acute viral infection. We find that CD8+ TRM across different tissues possess both shared and tissue-specific transcriptional and epigenetic signatures. Notably, Trm in the intestine and salivary gland express TGFb-induced genes and are maintained by ongoing TGFb signaling while those in the fat, kidney, and liver are not. By constructing transcriptional-regulatory networks for each Trm population, we identify the repressor Hic1 as a critical regulator of Trm differentiation, particularly for Trm of the small intestine. This study provides a framework for understanding how Trm adapt to distinct tissue environments and identifies tissue-specific transcriptional regulators that mediate these adaptations, informing strategies to enhance protective memory responses at the sites most vulnerable to infection.
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Project description:CD8+ memory T cells are critical components of protective immunity to intracellular pathogens and tumors. While many memory CD8+ T cells recirculate throughout the body, others remain lodged in tissues and guard common sites of pathogen entry. Contributions of the specific tissue environment to tissue-resident memory T cell (Trm) differentiation and homeostasis have been implicated but are not well understood. Here, we define the diversity of gene expression and genome accessibility by mouse CD8+ Trm populations in distinct organs and identify molecules critical for Trm generated in response to acute viral infection. We find that CD8+ TRM across different tissues possess both shared and tissue-specific transcriptional and epigenetic signatures. Notably, Trm in the intestine and salivary gland express TGFb-induced genes and are maintained by ongoing TGFb signaling while those in the fat, kidney, and liver are not. By constructing transcriptional-regulatory networks for each Trm population, we identify the repressor Hic1 as a critical regulator of Trm differentiation, particularly for Trm of the small intestine. This study provides a framework for understanding how Trm adapt to distinct tissue environments and identifies tissue-specific transcriptional regulators that mediate these adaptations, informing strategies to enhance protective memory responses at the sites most vulnerable to infection.
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Project description:CD8+ memory T cells are critical components of protective immunity to intracellular pathogens and tumors. While many memory CD8+ T cells recirculate throughout the body, others remain lodged in tissues and guard common sites of pathogen entry. Contributions of the specific tissue environment to tissue-resident memory T cell (Trm) differentiation and homeostasis have been implicated but are not well understood. Here, we define the diversity of gene expression and genome accessibility by mouse CD8+ Trm populations in distinct organs and identify molecules critical for Trm generated in response to acute viral infection. We find that CD8+ TRM across different tissues possess both shared and tissue-specific transcriptional and epigenetic signatures. Notably, Trm in the intestine and salivary gland express TGFb-induced genes and are maintained by ongoing TGFb signaling while those in the fat, kidney, and liver are not. By constructing transcriptional-regulatory networks for each Trm population, we identify the repressor Hic1 as a critical regulator of Trm differentiation, particularly for Trm of the small intestine. This study provides a framework for understanding how Trm adapt to distinct tissue environments and identifies tissue-specific transcriptional regulators that mediate these adaptations, informing strategies to enhance protective memory responses at the sites most vulnerable to infection.
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