Abstract

Although gammadelta T cells have been implicated in various aspects of the dermal wound healing process, their role in postburn wound healing processes has not been investigated. To study this, we subjected mice deficient in gammadelta T cells (ie, T-cell receptor delta gene [delta TCR]) and wild-type (WT; C57BL6J) mice to burn injury (25% TBSA) or sham treatment; skin samples were isolated 3 days later. Marked inflammation of the injury site was observed in WT mice but was markedly reduced in delta TCR mice. Postinjury fibroblast growth factor, platelet-derived growth factor granulocyte-colony stimulating factor levels, and nitrite/nitrate were elevated in skin samples from injured WT mice, whereas skin tissue levels of these growth factors and inflammatory mediators was significantly atteunuated in delta TCRmice. In conclusion, these findings support the concept that gammadelta T cells are important to postburn wound healing via the production of growth factors and, potentially, regulation of inducible nitric oxide synthase activation.

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