Burn injury induces a change in T cell homeostasis affecting preferentially CD4+ T cells.

Burn injuries are known to be associ- ated with altered immune functions, resulting in decreased resistance to subsequent infection. In the present study, we determined the in vivo changes in T cell homeostasis following burn in- jury. Two groups of mice were used: a sham-burn group receiving buprenorphine as an analgesic and a burn group receiving buprenorphine and sub- jected to burn injury on 20% of the total body surface area. Results showed an important de- crease in splenocytes following burn injury. This decrease persisted for 5 days and was followed, at day 10, by a 63% increase in numbers of cells. In vivo cell proliferation, as determined by the incor- poration of 5-bromo-2-dexoxyuridine, showed a significant increase of cycling splenocytes between days 2 and 10 after burn injury. The percentage of CD4 and CD8 T cells in the spleen was altered for 10 days after thermal injury. Analysis of naive (CD62L high CD44 low ) and effector/memory (CD62L low CD44 high ) T cells showed a percent de- crease, independent of the expression of CD4 or CD8 molecules. However, early activation mark- ers, such as CD69, were expressed only on CD4 T cells after a number of days following injury. Even with an activated phenotype, 10 days post- burn injury, CD4 naive T cells significantly in- creased spontaneous apoptosis, detected by using a fluorescent DNA-binding agent 7-amino-actinomy- cin D. CD8 T lymphocytes did not express early activation markers and were more resistant to ap- optosis. Using purified T cells, we have shown un- responsiveness at day 10. Overall, these results demonstrate that mechanisms of T cell homeostasis were perturbed following burn injury. However, after 10 days, this perturbation persisted only in CD4 T cells. J. Leukoc. Biol. 77: 000-000; 2005.