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Heuser-Loy, C.

Publications and source records attributed to Heuser-Loy, C..

2 recordsLinked to original sources

SCITRAM: a Single-cell Integrated transcription regulation modeler for predicting master transcription factors

Single-cell omics technologies have provided unprecedented access to molecular cell heterogeneity, revolutionizing our understanding of complex living systems. Although generating such type of data has become a streamlined process, data processing still relies on command-line driven tools, or commercial solutions. Furthermore, single-cell transcriptomics analysis is usually reduced to stratifying cells on the grounds of gene expression signatures, while deconvolving gene regulatory programs (and their associated master transcription factors) responsible for cell heterogeneity are not classically addressed with the available tools, or performed under different data processing platforms. Herein, we present SCITRAM (Single-Cell Integrated TRAnscription regulation Modeler), a user-friendly stand-alone computational solution for predicting master transcription factors from single-cell transcriptomics data. SCITRAM first reconstructs a primary gene regulatory network and subsequently uses this network as template to model transcriptional cascades driven by the in-silico activation of transcription factors identified within the system. We validated SCITRAM performance across a variety of cell fate transition events including T cell exhaustion during solid tumor treatment, lineage stratification during pancreatic endocrinogenesis, as well as nervous tissue formation in cerebral organoid models. Overall, SCITRAM provides an accessible and integrated platform for processing (large amounts of) single-cell transcriptomics data, enabling the investigation of transcriptional regulatory programs and their master transcription factors without requiring a command-line driven environment.

bioinformatics↗

Targeting ZC3H12C improves T cell persistence and antitumor function in adoptive T cell therapy

Adoptive T cell therapy (ACT) has achieved remarkable clinical responses in hematologic malignancies but remains limited by progressive T cell dysfunction under chronic antigen stimulation. Here, we identify ZC3H12C as a conserved feature of dysfunctional T cells and show that its disruption enhances the durability and antitumor activity of engineered T cells. By integrating single-cell chromatin accessibility and transcriptomic profiling of human tumor-infiltrating lymphocytes (TILs), we identified the ZC3H12C locus as selectively remodeled in exhausted T cells. ZC3H12C induction is largely absent across acute T cell activation contexts, indicating regulation that is specific to chronic antigen-driven dysfunction. Genetic disruption of ZC3H12C improves T cell expansion, cytotoxicity, and expression of effector molecules during repeated in vitro stimulation, translating into enhanced tumor control in vivo across both T cell receptor (TCR) and chimeric antigen receptor (CAR) T cell therapy platforms. Improved efficacy is observed in hematologic, solid, and metastatic tumor models and is accompanied by increased T cell persistence. Further, ZC3H12C is enriched in clinical pre-infusion CAR T cell products associated with non-response. Together, these findings identify ZC3H12C as a T cell dysfunction-specific target to improve ACT performance.

immunology↗