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Microbiota orchestrates monocyte reprogramming of the tumor microenvironment via type I IFN-STING axis to promote anticancer immunity

ABSTRACT: This study sets out to investigate the mechanisms by which gut microbiota controls the mononuclear phagocyte compartment of the tumor microenvironment to elicit effective anti-tumor responses. This dataset contains single-cell RNA sequencing data of leukocytes from murine subcutaneous EL4 lymphomas from mice with intact or absent microbiota.

ORGANISM(S): Mus musculus

PROVIDER: GSE181745 | GEO | 2021/10/09

REPOSITORIES: GEO

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Microbiota orchestrates monocyte reprogramming of the tumor microenvironment via type I IFN-STING axis to promote anticancer immunity

Project description:Microbiota orchestrates monocyte reprogramming of the tumor microenvironment via type I IFN-STING axis to promote anticancer immunity

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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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Project description:Our study had shown that DAC treatment enhanced immunogenecity of EL4 cells. To explore the mechanisms of DAC-induced tumor immunity, we carried out cDNA microarray analyses to compare the differential expression of genes between DAC and PBS treated EL4 cells. Two-condition experiment, PBS treated EL4 vs. Decitabine treated EL4 cells. Biological replicates: 3 PBS treated, 3 Decitabine treated, independently treatment and harvested. One replicate per array.

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Gene expression changes following demethylation by 5-aza-2'-deoxycytidine（decitabine, DAC）in mouse T cell lymphoma EL4 cells

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