Single cell RNA sequencing and TCR repertoire analysis of Adult T-cell Leukemia/Lymphoma (ATLL)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA801697 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR17809356_1.fastq.gz | Fastqsanger.gz | |||
| SRR17809356_2.fastq.gz | Fastqsanger.gz | |||
| SRR17809357_1.fastq.gz | Fastqsanger.gz | |||
| SRR17809357_2.fastq.gz | Fastqsanger.gz | |||
| SRR17809358_1.fastq.gz | Fastqsanger.gz |
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Project description:Temporal analysis of T-cell receptor (TCR) repertoire has been used to monitor treatment-induced changes in antigen-specific T cells in patients with cancer. However, lack of experimental model that allows the temporal analysis of TCR repertoire in same individual in homogeneous population limit the understanding of causal relationship between changes in TCR repertoire and antitumor responses. A bilateral tumor model, in which tumor cells were inoculated into the bilateral backs of mice, can be used for temporal analysis in TCR repertoire. In this study, we examined the prerequisite for this strategy: TCR repertoire are conserved between the bilateral tumor with same growth rate. The bilateral tumors with equivalent tumor size and draining lymph nodes (dLN) were collected 13 days after the tumor inoculation to analyze the TCR repertoire of CD4+ and CD8+ T cells. Most of the tumor-infiltrating T-cell clones were highly conserved between the bilateral tumors, and the extent of clonal expansion was equivalent. In addition, the similarity between bilateral tumors were equivalent to the heterogeneity in one side of the tumor. The similarity of TCR repertoire in the bilateral dLN was markedly lower than that of the tumor, suggesting that tumor-reactive T-cell clones induced independently in each dLN were integrated during recirculation and then infiltrated the tumor. These findings suggest that our bilateral tumor model is suitable for temporal monitoring of TCR repertoire to evaluate temporal and treatment-induced changes in tumor-reactive T-cell clones.
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Project description:We established HTLV-1/EBV co-infected cell lines from Adult T-cell Leukemia/Lymphoma (ATLL) patients, and found that they are derived from germinal center (GC) B-cells or transitional B-cells between GC-B-cells and memory B-cells by using gene expression profiling (GEP) analysis. Expression of CD25 and TSLC1, which are diagnostic markers of ATLL cells, were identified in the ATLL-derived B-cell lines as discriminators of EBV-imortalized cell lines, indicating that HTLV-1 infection leads to express CD25 and TSLC1.
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Project description:Adult T-cell leukemia-lymphoma (ATLL) is an HTLV-1-associated lymphoproliferative malignancy that is frequently fatal. We compared gene expression profiles (GEPs) of leukemic specimens from 9 patients with ATLL at the time of diagnosis and immediately after combination therapy with zidovudine (AZT) and interferon alpha (IFN). GEPs were also related to genetic aberrations determined by comparative genomic hybridization. We identified several genes anomalously over-expressed in the ATLL leukemic cells at the mRNA level, including LYN, CSPG2 and LMO2, with confirmation of LMO2 expression confirmed in ATLL cells at the protein level. In vivo AZT- and IFNa treatment evoked a marked induction of interferon-induced genes accompanied by repression of cell-cycles regulated genes including those encoding ribosomal proteins. Remarkably, patients not responding to IFNa/AZT differed most from responding patients in relative over expression of these same IFN-responsive genes, as well as components of the antigen processing and presentation apparatus. Demonstration of specific gene expression signatures associated with response to AZT-IFNa therapy may provide novel insights into the mechanisms of action in ATLL. compound_treatment_design
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Project description:Adult T-cell leukemia-lymphoma (ATLL) is an HTLV-1-associated lymphoproliferative malignancy that is frequently fatal. We compared gene expression profiles (GEPs) of leukemic specimens from 9 patients with ATLL at the time of diagnosis and immediately after combination therapy with zidovudine (AZT) and interferon alpha (IFN). GEPs were also related to genetic aberrations determined by comparative genomic hybridization. We identified several genes anomalously over-expressed in the ATLL leukemic cells at the mRNA level, including LYN, CSPG2 and LMO2, with confirmation of LMO2 expression confirmed in ATLL cells at the protein level. In vivo AZT- and IFNa treatment evoked a marked induction of interferon-induced genes accompanied by repression of cell-cycles regulated genes including those encoding ribosomal proteins. Remarkably, patients not responding to IFNa/AZT differed most from responding patients in relative over expression of these same IFN-responsive genes, as well as components of the antigen processing and presentation apparatus. Demonstration of specific gene expression signatures associated with response to AZT-IFNa therapy may provide novel insights into the mechanisms of action in ATLL.
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