ENAapplication/xmlftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR610/006/ERR6109006/ERR6109006.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR610/008/ERR6109008/ERR6109008.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR610/007/ERR6109007/ERR6109007.fastq.gzftp://ftp.sra.ebi.ac.uk/vol1/fastq/ERR610/009/ERR6109009/ERR6109009.fastq.gzprimaryOK200GenomicsUNIVERSITY OF TASMANIAhttps://www.ebi.ac.uk/ena/browser/view/PRJEB45867xref:EuropePMC:PMC9579919MHC-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.ENAfalseRegulation of MHC-I and MHC-II expression by CIITA in transmissible devil facial tumour cellsTranscriptomic analysis of DFT1 and DFT2 cells with overexpression of CIITA2022-01-052022-01-05PRJEB45867