Journal
NATURE IMMUNOLOGY
Volume 6, Issue 1, Pages 73-79Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1152
Keywords
-
Categories
Funding
- NIAID NIH HHS [T32AI36964, T32AI07244] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI007244, R01AI036964] Funding Source: NIH RePORTER
Ask authors/readers for more resources
A fine balance between rates of proliferation and apoptosis in the skin provides a defensive barrier and a mechanism for tissue repair after damage. Vgamma3(+) dendritic epidermal T cells (DETCs) are primary modulators of skin immune responses. Here we show that DETCs both produce and respond to insulin-like growth factor 1 (IGF-1) after T cell receptor stimulation. Mice deficient in DETCs had a notable increase in epidermal apoptosis that was abrogated by the addition of DETCs or IGF-1. Furthermore, DETC-deficient mice had reduced IGF-1 receptor activation at wound sites. These findings indicate critical functions for DETC-mediated IGF-1 production in regulating skin homeostasis and repair.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available