Journal
JOURNAL OF EXPERIMENTAL MEDICINE
Volume 201, Issue 8, Pages 1269-1279Publisher
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20042057
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Funding
- NIAID NIH HHS [T32 AI007244, R01 AI036964, 5T43AI-07244, AI-32751, AI-36964] Funding Source: Medline
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Nonhealing wounds are a major complication of diseases such as diabetes and rheumatoid arthritis. For efficient tissue repair, inflammatory cells must infiltrate into the damaged tissue to orchestrate wound closure. Hyaluronan is involved in the inflammation associated with wound repair and binds the surface of leukocytes infiltrating damaged sites. Skin gamma delta T cells play specialized roles in keratinocyte proliferation during wound repair. Here, we show that gamma delta T cells are required for hyaluronan deposition in the extracellular matrix (ECM) and subsequent macrophage infiltration into wound sites. We describe a novel mechanism of control in which gamma delta T cell-derived keratinocyte growth factors induce epithelial cell production of hyaluronan. In turn, hyaluronan recruits macrophages to the site of damage. These results demonstrate a novel function for skin gamma delta T cells in inflammation and provide a new perspective on T cell regulation of ECM molecules.
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