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γδ T‐cell dysregulation in the cutaneous diabetic environment
Author(s) -
Taylor Kristen R.,
Mills Robyn E.,
Jameson Julie M.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1065.10
Subject(s) - wound healing , t cell , il 2 receptor , t cell receptor , immune system , immunology , medicine , diabetes mellitus , receptor , keratinocyte growth factor , microbiology and biotechnology , biology , endocrinology , growth factor
Skin γδ T‐cells are specialized intraepithelial lymphocytes that express a canonical γδ T‐cell receptor (TCR), which recognizes stressed or damaged epithelial cells. Once activated, skin γδ T‐cells release cytokines and growth factors that facilitate cutaneous wound healing. In diabetes, wound healing is delayed and patients often suffer from chronic infections. We hypothesize that skin γδ T‐cells are dysregulated in diabetes, contributing to complications in wound healing. Using the leptin receptor deficient mouse model of Type 2 diabetes, we have determined that skin γδ T‐cell homeostasis is altered in the diabetic environment. Skin γδ T‐cells in diabetic mice display decreased levels of T‐cell activation markers including CD69, CD25 and the γδ TCR, indicating a decreased activation status. Following the onset of diabetes, the number of skin γδ T‐cells decrease two‐fold. In vivo wound healing assays reveal that diabetic γδ T‐cells have delayed rounding following wounding, suggesting an inability to respond to epithelial cell damage. Taken together, our studies suggest that the diabetic environment has negative effects on the activation status of skin γδ T‐cells and ultimately renders them unable to properly respond to damaged epithelial cells. Alterations in skin γδ T‐cell function may influence the production of growth factors and contribute to immune and repair deficiencies in diabetic patients.