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Related Concept Videos

Chromatin Modification in iPS Cells01:32

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Chromatin modification alters gene expression; therefore, scientists can add histone-modifying enzymes, histone variants, and chromatin remodeling complexes to somatic cells to aid reprogramming into pluripotent stem (iPS) cells.
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Epigenetics is the study of inherited changes in a cell's phenotype without changing the DNA sequences. It provides a form of memory for the differential gene expression pattern to maintain cell lineage, position-effect variegation, dosage compensation, and maintenance of chromatin structures such as telomeres and centromeres. For example, the structure and location of the centromere on chromosomes are epigenetically inherited. Its functionality is not dictated or ensured by the underlying...
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Chromatin is the massive complex of DNA and proteins packaged inside the nucleus. The complexity of chromatin folding and how it is packaged inside the nucleus greatly influences  access to genetic information. Generally, the nucleus' periphery is considered transcriptionally repressive, while the cell's interior is considered a transcriptionally active area. 
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An Integrated Platform for Genome-wide Mapping of Chromatin States Using High-throughput ChIP-sequencing in Tumor Tissues
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Chromatin states define tumour-specific T cell dysfunction and reprogramming.

Mary Philip1, Lauren Fairchild2,3, Liping Sun4

  • 1Immunology Program, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA.

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|May 18, 2017
PubMed
Summary
This summary is machine-generated.

Tumour-infiltrating CD8 T cells exist in two states: one plastic and reprogrammable, the other fixed and resistant. Identifying surface markers predicts which dysfunctional T cells can be therapeutically reprogrammed for cancer immunotherapy.

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Area of Science:

  • Immunology
  • Cancer Biology
  • Epigenetics

Background:

  • Tumour-specific CD8 T cells in solid tumours often become dysfunctional, hindering anti-tumour immune responses.
  • The epigenetic mechanisms governing T cell dysfunction and their susceptibility to reprogramming therapies, such as immune checkpoint blockade, remain poorly understood.

Purpose of the Study:

  • To investigate the epigenetic regulation of CD8 T cell dysfunction in tumours.
  • To identify distinct T cell states within tumours and their potential for therapeutic reprogramming.
  • To discover surface markers that predict T cell reprogrammability for cancer immunotherapy.

Main Methods:

  • Analysis of chromatin states in mouse tumour-infiltrating CD8 T cells.
  • Identification of surface markers distinguishing T cell subpopulations.
  • Comparison of mouse and human tumour-infiltrating CD8 T cells.

Main Results:

  • CD8 T cells in mouse tumours differentiate into two discrete chromatin states: a plastic, reprogrammable dysfunctional state and a fixed, resistant dysfunctional state.
  • Specific surface markers were identified that differentiate reprogrammable from non-reprogrammable PD1hi dysfunctional CD8 T cells.
  • These identified surface markers are also present on human PD1hi tumour-infiltrating CD8 T cells.

Conclusions:

  • Epigenetic programs dictate distinct dysfunctional CD8 T cell states within tumours, influencing their therapeutic potential.
  • Surface markers can predict the reprogrammability of dysfunctional CD8 T cells, offering a biomarker for cancer immunotherapy.
  • Understanding these epigenetic and surface marker profiles is crucial for developing effective immunotherapies.