Your browser doesn't support javascript.
loading
IL-33 Signaling Alters Regulatory T Cell Diversity in Support of Tumor Development.
Li, Amy; Herbst, Rebecca H; Canner, David; Schenkel, Jason M; Smith, Olivia C; Kim, Jonathan Y; Hillman, Michelle; Bhutkar, Arjun; Cuoco, Michael S; Rappazzo, C Garrett; Rogers, Patricia; Dang, Celeste; Jerby-Arnon, Livnat; Rozenblatt-Rosen, Orit; Cong, Le; Birnbaum, Michael; Regev, Aviv; Jacks, Tyler.
Affiliation
  • Li A; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA; Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA; Harvard Medical School, 25 Shattuck Street, Bost
  • Herbst RH; Harvard Medical School, 25 Shattuck Street, Boston, MA 02115, USA; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
  • Canner D; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA; Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA.
  • Schenkel JM; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA; Department of Pathology, Brigham and Women's Hospital, Boston, MA 02115, USA.
  • Smith OC; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA.
  • Kim JY; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA.
  • Hillman M; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA.
  • Bhutkar A; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA.
  • Cuoco MS; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
  • Rappazzo CG; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA; Department of Biological Engineering, Massachusetts Institute of Technology, 21 Ames Street, Cambridge, MA 02142, USA.
  • Rogers P; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
  • Dang C; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA.
  • Jerby-Arnon L; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
  • Rozenblatt-Rosen O; Broad Institute of MIT and Harvard, 415 Main Street, Cambridge, MA 02142, USA.
  • Cong L; Department of Pathology, Stanford University, Stanford, CA 94305, USA; Department of Genetics, Stanford University, Stanford, CA 94305, USA.
  • Birnbaum M; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA; Department of Biological Engineering, Massachusetts Institute of Technology, 21 Ames Street, Cambridge, MA 02142, USA.
  • Regev A; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA; Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA; Broad Institute of MIT and Harvard, 415 Main Str
  • Jacks T; David H. Koch Institute for Integrative Cancer Research, Massachusetts Institute of Technology, 500 Main Street, Cambridge, MA 02139, USA; Department of Biology, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, MA 02139, USA; Howard Hughes Medical Institute, Massachusetts I
Cell Rep ; 29(10): 2998-3008.e8, 2019 12 03.
Article in En | MEDLINE | ID: mdl-31801068
ABSTRACT
Regulatory T cells (Tregs) can impair anti-tumor immune responses and are associated with poor prognosis in multiple cancer types. Tregs in human tumors span diverse transcriptional states distinct from those of peripheral Tregs, but their contribution to tumor development remains unknown. Here, we use single-cell RNA sequencing (RNA-seq) to longitudinally profile dynamic shifts in the distribution of Tregs in a genetically engineered mouse model of lung adenocarcinoma. In this model, interferon-responsive Tregs are more prevalent early in tumor development, whereas a specialized effector phenotype characterized by enhanced expression of the interleukin-33 receptor ST2 is predominant in advanced disease. Treg-specific deletion of ST2 alters the evolution of effector Treg diversity, increases infiltration of CD8+ T cells into tumors, and decreases tumor burden. Our study shows that ST2 plays a critical role in Treg-mediated immunosuppression in cancer, highlighting potential paths for therapeutic intervention.
Subject(s)
Key words
Fulltext
Print
XML
PubMed Links
Search on Google

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Signal Transduction / T-Lymphocytes, Regulatory / Interleukin-33 Limits: Animals Language: En Journal: Cell Rep Year: 2019 Type: Article
Fulltext
Print
XML
PubMed Links
Search on Google

Full text: 1 Collection: 01-internacional Database: MEDLINE Main subject: Signal Transduction / T-Lymphocytes, Regulatory / Interleukin-33 Limits: Animals Language: En Journal: Cell Rep Year: 2019 Type: Article