Effect of TGFb on TCR-induced OT-I T cell gene expression
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA846784 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19575042_1.fastq.gz | Fastqsanger.gz | |||
| SRR19575042_2.fastq.gz | Fastqsanger.gz | |||
| SRR19575043_1.fastq.gz | Fastqsanger.gz | |||
| SRR19575043_2.fastq.gz | Fastqsanger.gz | |||
| SRR19575044_1.fastq.gz | Fastqsanger.gz |
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Project description:In mice and humans, an immature CD4-CD8- double negative (DN) thymocyte subset expresses early, mature αβTCR. These early αβTCR+ DN (EADN) cells are susceptible to leukemogenesis in both species. Using the OT-1 TCR transgenic system to model EADN-stage αβ TCR expression, we found that EADN cells show coreceptor-independent reactivity to MHC, and their TCR:MHC dependent signals can drive T-ALL transformation. We generated gene expression data from OT-1 leukemic cells and assessed their developmental stage by comparing to wild-type thymocyte subsets.
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Project description:We report the application of TCRβ sequencing to understand T cell repertoire of matched blood and tumor samples pre and post treatment in EG7.OVA tumor bearing mice with OT-1 cell transfer. TCRβ sequencing demonstrated that OT-1 (CASSRANYEQYF) was the most abundant T-cell clone in both blood and tumors of mRBC‑OVA-4-1BBL-IL-12 treated mice. To investigate the effects of mRBC‑OVA-4-1BBL-IL-12 on immune memory, the T cell repertoire was also analyzed before and after EG7.OVA and EL4 tumor rechallenge in cured and treatment-naive mice. TCRβ sequencing on T cells in peripheral blood showed that OT-1 clones increased in frequency after EG7.OVA challenge in previously cured mice. OT-1 frequency did not increase in treatment-naïve mice after tumor challenge, indicating that the tumor alone is insufficient to drive OT-1 cell expansion. We also evaluated the frequencies of unique TCRβ sequences in T cell clones that significantly expanded post EL4 challenge (EL4 responsive TCR). Increased frequency of EL4-responsive TCRs upon each tumor challenge (EG7.OVA and EL4) was associated with complete responders (mice that rejected EL4 challenge), suggesting that T-cell-mediated protection against parental tumor antigens was generated prior to EL4 challenge. Partial responders (delayed tumor growth compared with naïve mice) had increases in EL4-responsive TCR frequencies after EL4 challenge but not during the EG7.OVA rechallenge, whereas the non-responder (tumor growth similar to naïve mice) had minimal increases in TCR frequencies upon EL4 challenge. Overall, the ability to control EL4 tumors correlated with the expansion of EL4-responsive TCR clones.
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