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Published online before print November 12, 2004

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0703314

Received for publication July 4, 2003.
Revised September 20, 2004.
Accepted for publication October 4, 2004.

Article

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

Julie Patenaude ^*, Michele D’Elia ^*, Claudine Hamelin ^*, Dominique Garrel , and Jacques Bernier ^*@

*INRS-Institut Armand-Frappier, Pointe-Claire, Quebec, Canada; and Centre hospitalier de l’Université de Montréal (CHUM)-Hôtel-Dieu, Centre des Grands Brûlés, Quebec, Canada

^@ To whom correspondence should be addressed. E-mail: jacques.bernier{at}inrs- sante.uquebec.ca.

	Abstract

Burn injuries are known to be associated 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 injury. Two groups of mice were used: a sham-burn group receiving buprenorphine as an analgesic and a burn group receiving buprenorphine and subjected to burn injury on 20% of the total body surface area. Results showed an important decrease 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 incorporation 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 decrease, independent of the expression of CD4 or CD8 molecules. However, early activation markers, 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 increased spontaneous apoptosis, detected by using a fluorescent DNA-binding agent 7-amino-actinomycin D. CD8⁺ T lymphocytes did not express early activation markers and were more resistant to apoptosis. Using purified T cells, we have shown unresponsiveness 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.

Key Words: apoptosis • anergy • macrophages • trauma • mice

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				J. W. Smith, R. L. Gamelli, S. B. Jones, and R. Shankar Immunologic responses to critical injury and sepsis. J Intensive Care Med, May 1, 2006; 21(3): 160 - 172. [Abstract] [PDF]