ena-STUDY-UNIVERSITY OF TASMANIA-23-06-2021-04:41:29:726-1087
Transcriptomic analysis of DFT1 and DFT2 cells with overexpression of CIITA
MHC-I and MHC-II molecules are critical components of antigen presentation and T cell immunity to pathogens and cancer. The transmissible devil facial tumour (DFT) cells that cause Tasmanian devil facial tumour disease (DFTD) exploit MHC-I pathways to overcome immunological anti-tumour and allogeneic barriers. MHC-II expression is crucial for CD4+ T cell activation and is primarily confined to haematopoietic professional antigen presenting cells. We discovered that the MHC-II transactivator, CIITA, can induce MHC-II expression in non-haematopoietic DFT cells. Transcriptomic analysis of DFT1 and DFT2 cell lines revealed that CIITA upregulates several genes of the MHC-I and MHC-II pathways, resulting in protein expression of MHC-I and MHC-II complexes. Each dataset was generated by single-end 100-base pair sequencing on the Illumina NovaSeq 6000 platform. Data is provided in raw FASTQ format.
MHC-I and MHC-II molecules are critical components of antigen presentation and T cell immunity to pathogens and cancer. The transmissible devil facial tumour (DFT) cells that cause Tasmanian devil facial tumour disease (DFTD) exploit MHC-I pathways to overcome immunological anti-tumour and allogeneic barriers. MHC-II expression is crucial for CD4+ T cell activation and is primarily confined to haematopoietic professional antigen presenting cells. We discovered that the MHC-II transactivator, CIITA, can induce MHC-II expression in non-haematopoietic DFT cells. Transcriptomic analysis of DFT1 and DFT2 cell lines revealed that CIITA upregulates several genes of the MHC-I and MHC-II pathways, resulting in protein expression of MHC-I and MHC-II complexes. Each dataset was generated by single-end 100-base pair sequencing on the Illumina NovaSeq 6000 platform. Data is provided in raw FASTQ format.