Rebecca H. Herbst
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Previous Organizations / Institutes
The organizations / institutes from the scholar's other articles in the past ten years
Research Subjects
Research Interests
Rebecca H. Herbst has a total of 29 co-authors. Here are the top co-authors by number of shared publications:
- Aviv Regev
Department of Biology, Massachusetts Institute of Technology, Cambridge, USA
2 shared publications - Orit Rozenblatt-Rosen
Klarman Cell Observatory, Broad Institute of MIT and Harvard, Cambridge, MA, 02142, USA
2 shared publications - Ahram Jang
Department of Pathology, Boston Children's Hospital, Boston, MA 02115, USA
1 shared publication - Amy Li
David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
1 shared publication - Arjun Bhutkar
Koch Institute for Integrative Cancer Research at MIT
1 shared publication - Celeste Q Dang
David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology
1 shared publication
Latest Publications
- Open Access
A cellular and spatial map of the choroid plexus across brain ventricles and ages
The choroid plexus (ChP), located in each brain ventricle, produces cerebrospinal fluid (CSF) and forms the blood-CSF barrier, but is under-characterized. Here, we combine single cell RNA-Seq and spatial mapping of RNA and proteins to construct an atlas of each ChP in the developing and adult mouse brain. Each ChP comprises of epithelial, endothelial, mesenchymal, immune, neuronal, and glial cells, with distinct subtypes, differentiation states and anatomical locations. Epithelial, fibroblast, and macrophage populations had ventricle-specific, regionalized gene expression programs across the developing brain. Key cell types are retained in adult, with loss of developmental signatures and maturation of ventricle-specific regionalization in the epithelial cells. Expression of cognate ligand-receptor pairs across cell subtypes suggests substantial cell-cell interactions within the ChP. Our atlas sheds new light on the development and function of the ChP brain barrier system, and will facilitate future studies on its role in brain development, homeostasis and disease.
Open AccessA cellular and spatial map of the choroid plexus across brain ventricles and ages
The choroid plexus (ChP), located in each brain ventricle, produces cerebrospinal fluid (CSF) and forms the blood-CSF barrier, but is under-characterized. Here, we combine single cell RNA-Seq and spatial mapping of RNA and proteins to construct an atlas of each ChP in the developing and adult mouse brain. Each ChP comprises of epithelial, endothelial, mesenchymal, immune, neuronal, and glial cells, with distinct subtypes, differentiation states and anatomical locations. Epithelial, fibroblast, and macrophage populations had ventricle-specific, regionalized gene expression programs across the developing brain. Key cell types are retained in adult, with loss of developmental signatures and maturation of ventricle-specific regionalization in the epithelial cells. Expression of cognate ligand-receptor pairs across cell subtypes suggests substantial cell-cell interactions within the ChP. Our atlas sheds new light on the development and function of the ChP brain barrier system, and will facilitate future studies on its role in brain development, homeostasis and disease.
- Open Access
Longitudinal single cell profiling of regulatory T cells identifies IL-33 as a driver of tumor immunosuppression
Regulatory T cells (T regs ) can impair anti-tumor immune responses and are associated with poor prognosis in multiple cancer types. T regs in human tumors span diverse transcriptional states distinct from those of peripheral T regs , but their contribution to tumor development remains unknown. Here, we used single cell RNA-Seq to longitudinally profile conventional CD4 + T cells (T conv ) and T regs in a genetic mouse model of lung adenocarcinoma. Tissue-infiltrating and peripheral CD4 + T cells differed, highlighting divergent pathways of activation during tumorigenesis. Longitudinal shifts in T reg heterogeneity suggested increased terminal differentiation and stabilization of an effector phenotype over time. In particular, effector T regs had enhanced expression of the interleukin 33 receptor ST2. T reg -specific deletion of ST2 reduced effector T regs , increased infiltration of CD8 + T cells into tumors, and decreased tumor burden. Our study shows that ST2 plays a critical role in T reg -mediated immunosuppression in cancer, highlighting new potential paths for therapeutic intervention.
Open AccessLongitudinal single cell profiling of regulatory T cells identifies IL-33 as a driver of tumor immunosuppression
Regulatory T cells (T regs ) can impair anti-tumor immune responses and are associated with poor prognosis in multiple cancer types. T regs in human tumors span diverse transcriptional states distinct from those of peripheral T regs , but their contribution to tumor development remains unknown. Here, we used single cell RNA-Seq to longitudinally profile conventional CD4 + T cells (T conv ) and T regs in a genetic mouse model of lung adenocarcinoma. Tissue-infiltrating and peripheral CD4 + T cells differed, highlighting divergent pathways of activation during tumorigenesis. Longitudinal shifts in T reg heterogeneity suggested increased terminal differentiation and stabilization of an effector phenotype over time. In particular, effector T regs had enhanced expression of the interleukin 33 receptor ST2. T reg -specific deletion of ST2 reduced effector T regs , increased infiltration of CD8 + T cells into tumors, and decreased tumor burden. Our study shows that ST2 plays a critical role in T reg -mediated immunosuppression in cancer, highlighting new potential paths for therapeutic intervention.