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Replicative cell senescence is a property of cells that allows them to divide a finite number of times throughout the organism's lifespan while preventing excessive proliferation. Replicative senescence is associated with the gradual loss of the telomere — short, repetitive DNA sequences found at the end of the chromosomes. Telomeres are bound by a group of proteins to form a protective cap on the ends of chromosomes. Embryonic stem cells express telomerase — an enzyme that adds...
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When T cells with CD4 markers are activated, they give rise to two types of effector cells: helper T cells and regulatory T cells. Meanwhile, T cells with CD8 markers differentiate into effector cytotoxic T cells. The differentiation of CD4 T cells into helper T cell subsets, such as Th1, Th2, and Th17 cells, is dependent on the antigen type, antigen-presenting cell, and regulatory cytokines.
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Induction and Validation of Cellular Senescence in Primary Human Cells
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Single-cell transcriptomics reveals a senescence-associated IL-6/CCR6 axis driving radiodermatitis.

Mor Paldor1, Orr Levkovitch-Siany1, Dana Eidelshtein1

  • 1The Goldyne-Savad Institute of Gene Therapy, Hadassah Hebrew University Hospital, Jerusalem, Israel.

EMBO Molecular Medicine
|July 5, 2022
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Summary

Radiation therapy can cause skin side effects like hair loss and dermatitis. This study identifies key molecular pathways, including IL-6 and IL-1 signaling, driving these radiotherapy complications.

Keywords:
CCR6IL-6alopeciaradiodermatitissenescence

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Area of Science:

  • Oncology
  • Dermatology
  • Immunology

Background:

  • Irradiation-induced alopecia and dermatitis (IRIAD) are common radiotherapy side effects.
  • The underlying molecular mechanisms of IRIAD are not well understood.

Purpose of the Study:

  • To elucidate the molecular and cellular basis of irradiation-induced alopecia and dermatitis (IRIAD).
  • To identify potential therapeutic targets for managing radiotherapy-induced skin damage.

Main Methods:

  • Single-cell RNA sequencing (scRNA-seq) of irradiated skin cells.
  • Genetic ablation studies in IL-6 knockout (IL-6-/-) and IL-1 receptor knockout (IL-1R-/-) mice.
  • Molecular inhibition studies and CCR6 knockout (CCR6-/-) mouse models.
  • Bioinformatics analysis to identify signaling pathways and cell types involved.

Main Results:

  • Senescence-associated IL-6 and IL-1 signaling, along with IL-17 upregulation and CCR6+ immune cell migration, were identified as key drivers of IRIAD.
  • IL-6 signaling was localized to hair follicles, basal keratinocytes, and dermal fibroblasts.
  • Genetic or molecular blockade of IL-6, IL-1, or CCR6 pathways significantly ameliorated IRIAD.
  • IL-6 deficiency reduced IL-17, IL-22, CCL20, and CCR6; CCR6 deficiency reduced IL-6, IL-17, CCL3, and MHC, indicating cellular cross-talk.

Conclusions:

  • Targeting IL-6, IL-1, and CCR6-mediated pathways can mitigate IRIAD.
  • Topical Janus kinase inhibitors and cyclosporine show therapeutic potential for radiotherapy-induced skin side effects.