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Immune regulation

TSLP: not just skin deep

Nature Reviews Immunology volume 8, pages 492–493 (2008)Cite this article

The authors sought to identify the reason for early lethality of mutant mice in which skin keratinocytes are deficient in either Notch1 and Notch2 or in the γ-secretase enzyme that is required for Notch activation. Notch signalling pathways have crucial roles in directing cell fate and function in many different tissues and, in the skin, their disruption leads to barrier defects and impaired skin differentiation. In addition to having skin-barrier defects, both mutant strains of mice had an increase in the number of circulating white blood cells, which increased exponentially in the first few weeks of life.

Closer examination of peripheral immune-cell subsets in the mutant mice revealed that pre-B-cell and immature B-cell populations were preferentially expanded. This B-cell lymphoproliferative disease led to enlargement of the spleen, B-cell infiltration of vital organs and death around the time of weaning. If the B-cell lymphoproliferative disease was prevented by irradiation and bone-marrow transplantation of wild-type cells, the mutant mice lived longer but still succumbed to death due to complications of their skin-barrier defects.

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ORIGINAL RESEARCH PAPER

  1. Demehri, S. et al. Notch-deficient skin induces a lethal systemic B-lymphoproliferative disorder by secreting TSLP, a sentinel for epidermal integrity. PLoS Biol. 6, e123 (2008)

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  1. Sarah Allan
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Allan, S. TSLP: not just skin deep. Nat Rev Immunol 8, 492–493 (2008). https://doi.org/10.1038/nri2363

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  • DOI: https://doi.org/10.1038/nri2363

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