• Martin G Schwacha and Tanjanika Daniel.
• Department of Surgery, Division of Trauma and Emergency Surgery, University of Texas Health Science Center at San Antonio, Mail Code 7740, 7703 Floyd Curl Drive, San Antonio, TX 78229-3900, USA. Schwacha@uthscsa.edu
• Cytokine. 2008 Dec 1; 44 (3): 328-34.

AbstractBurn injury is associated with profound inflammation and activation of the innate immune system involving gammadelta T-cells. Similarly, Toll-like receptors (TLR) are associated with activation of the innate immune response; however, it is unclear whether TLR expression is altered in gammadelta T-cells after major burn injury. To study this, male C57BL/6 mice were subjected to burn injury (25% TBSA) and 1 or 7 days thereafter, blood and spleen cells were isolated and subjected to FACs analysis for TLRs and other phenotypic markers (gammadelta TCR, alphabeta TCR, CD69, CD120b). A marked increase in the number of circulating gammadelta T-cells was observed at 24h post-burn (14% vs. 4%) and a higher percentage of these cells expressed TLR-2. TLR-4 expression was also increased post-burn, but to a lesser degree. These changes in TLR expression were not associated with altered CD69 or CD120b expression in gammadelta T-cells. The mobilization of, and increased TLR expression in, gammadelta T-cells was transient, as phenotypic changes were not evident at 7 days post-burn or in gammadelta T-cells from the circulation or spleen. The increases in TLR expression were not observed in alphabeta T-cells after burn injury. In conclusion, 24h after burn injury mobilization of gammadelta T-cells with increased TLR expression was observed. This finding suggests that this unique T-cell population is critical in the innate immune response to injury, possibly through the recognition of danger signals by TLRs.

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