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Trends Neurosci. 2016 Jul;39(7):463-471. doi: 10.1016/j.tins.2016.04.005. Epub 2016 May 4.

Taking a Toll on Self-Renewal: TLR-Mediated Innate Immune Signaling in Stem Cells.

Author information

1
Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, USA.
2
Department of Cellular and Molecular Medicine, Lerner Research Institute, Cleveland Clinic, Cleveland, OH, USA; Department of Molecular Medicine, Cleveland Clinic Lerner College of Medicine of Case Western Reserve University, Cleveland, OH, USA; Rose Ella Burkhardt Brain Tumor and Neuro-Oncology Center, Cleveland Clinic, Cleveland, OH, USA; Case Comprehensive Cancer Center, Cleveland, OH, USA. Electronic address: lathiaj@ccf.org.

Abstract

Innate immunity has evolved as the front-line cellular defense mechanism to acutely sense and decisively respond to microenvironmental alterations. The Toll-like receptor (TLR) family activates signaling pathways in response to stimuli and is well-characterized in both resident and infiltrating immune cells during neural inflammation, injury, and degeneration. Innate immune signaling has also been observed in neural cells during development and disease, including in the stem and progenitor cells that build the brain and are responsible for its homeostasis. Recently, the activation of developmental programs in malignant brain tumors has emerged as a driver for growth via cancer stem cells. In this review we discuss how innate immune signaling interfaces with stem cell maintenance in the normal and neoplastic brain.

KEYWORDS:

Toll-like receptor; cancer stem cells; glioblastoma; neural progenitor cells

PMID:
27155992
DOI:
10.1016/j.tins.2016.04.005
[Indexed for MEDLINE]

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