Effect of recombinant human CD26/DPPIV protein or Sitagliptin (DPPIV enzyme inhibitor) on CD3 T cells at day 2 after in vitro cell culture
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE294787 | GEO | 2026/01/10
REPOSITORIES: GEO
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Project description:Transcriptomic profiling of ovine skin lymph dendritic cell subsets CD26+ and CD26- compared to total enriched lymph dendritic cells. CD26+ and CD26- dendritic cells (DC) from sheep skin lymph were sorted by flow cytometry and were analysed for their transcriptomic profile. We demonstrate that the minor sheep CD26+ skin lymph DC subset shares significant transcriptomic similarities with mouse CD8a+ and human BDCA3+ DC. This allowed the identification of a common set of phenotypic characteristics for CD8a-like DC in the 3 mammalian species, i.e. SIRPlo, CADM1hi, CLEC9Ahi, DEC205hi, XCR1hi. Compared to CD26- DC, the sheep CD26+ DC show (1) potent stimulation of allogeneic naive CD8+ T cells with high selective induction of the Ifn-gamma and Il22 genes; (2) dominant efficacy in activating specific CD8+ T cells against exogenous soluble antigen; (3) selective expression of functional pathways associated to high capacity for antigen cross-presentation.
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Project description:Cancer-associated fibroblasts (CAFs) are abundantly present in the microenvironment of virtually all tumors and strongly impact tumor progression. Despite increasing insight into their function and heterogeneity, little is known regarding the origin of CAFs. Understanding the origin of CAF heterogeneity is needed to develop successful CAF-based targeted therapies. Through various transplantation studies in mice we determined that CAFs in both invasive lobular breast cancer and triple negative breast cancer originate from mammary tissue-resident normal fibroblasts (NFs). Single-cell transcriptomics, in vivo tracing and in vitro studies revealed the transition of CD26+ and CD26- NF populations into inflammatory CAFs (iCAFs) and myofibroblastic CAFs (myCAFs), respectively. In vitro functional assays showed that CD26+ NFs transition into pro-tumorigenic iCAFs which recruit myeloid cells in a CXCL12-dependent manner and enhance tumor cell invasion via matrix-metalloproteinase (MMP) activity. Together, our data show that CD26+ and CD26- NFs transform into distinct CAF subpopulations in breast cancer.
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Project description:Cancer-associated fibroblasts (CAFs) are abundantly present in the microenvironment of virtually all tumors and strongly impact tumor progression. Despite increasing insight into their function and heterogeneity, little is known regarding the origin of CAFs. Understanding the origin of CAF heterogeneity is needed to develop successful CAF-based targeted therapies. Through various transplantation studies in mice we determined that CAFs in both invasive lobular breast cancer and triple negative breast cancer originate from mammary tissue-resident normal fibroblasts (NFs). Single-cell transcriptomics, in vivo tracing and in vitro studies revealed the transition of CD26+ and CD26- NF populations into inflammatory CAFs (iCAFs) and myofibroblastic CAFs (myCAFs), respectively. In vitro functional assays showed that CD26+ NFs transition into pro-tumorigenic iCAFs which recruit myeloid cells in a CXCL12-dependent manner and enhance tumor cell invasion via matrix-metalloproteinase (MMP) activity. Together, our data show that CD26+ and CD26- NFs transform into distinct CAF subpopulations in breast cancer.
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