<HashMap><database>GEO</database><file_versions><headers><Content-Type>application/xml</Content-Type></headers><body><files><Other>ftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE223nnn/GSE223442/</Other></files><type>primary</type></body><statusCode>OK</statusCode><statusCodeValue>200</statusCodeValue></file_versions><scores/><additional><omics_type>Transcriptomics</omics_type><species>Mus musculus</species><gds_type>Expression profiling by high throughput sequencing</gds_type><full_dataset_link>https://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE223442</full_dataset_link><repository>GEO</repository><entry_type>GSE</entry_type></additional><is_claimable>false</is_claimable><name>scRNA seq of blood cells from Ikka or Stat3 inducible ablated mouse with fungi treatment</name><description>Diverse taxa of fungus kingdom are part of cancer related microbiota but which fungi induce pro-tumor immune responses and whether they impact specific cancer pathways are unclear. Here, we use Cladosporium cladosporioides to orally infect wildtype mice or mice lacking Ikka or Stat3/Ikka in epithelial stem cells. This infection promotes systemic inflammation, acidic oral milieu with Proteobacteria expansion, and oral and skin squamous cell carcinoma (SCC) development. Double Stat3 and Ikka deletions reverse these phenotypes. We found in the serum of mouse, C. cladosporioides induces IL-17a and Il-1b production. To determine which cells contribute the upregulated level of Il-1b and Il17a in the blood under fungi treament, we conducted 10x genomics single cell RNA sequencing on mRNA in blood cells from WT, Ikka or Stat3/Ikka inducible ablated mice with fungi treatment (Cladosporium cladosporioides).</description><dates><publication>2026/08/20</publication></dates><accession>GSE223442</accession><cross_references><GSM>GSM6953392</GSM><GSM>GSM6953393</GSM><GSM>GSM6953394</GSM><GPL>24247</GPL><GSE>223442</GSE><taxon>Mus musculus</taxon></cross_references></HashMap>