Patenaude, Julie; D'Elia, Michele; Hamelin, Claudine; Garrel, Dominique et Bernier, Jacques ORCID: https://orcid.org/0000-0002-0594-5922 (2005). Burn injury induces a change in T cell homeostasis affecting preferentially CD4+ T cells Journal of Leukocyte Biology , vol. 77 , nº 2. pp. 141-150. DOI: 10.1189/jlb.0703314.
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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 number 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 (CD62Lhigh CD44low) and effector/memory (CD62Llow CD44high) 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.
Type de document: | Article |
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Mots-clés libres: | Apoptosis; anergy; macrophages; trauma; mice |
Centre: | Centre INRS-Institut Armand Frappier |
Date de dépôt: | 11 nov. 2024 20:17 |
Dernière modification: | 11 nov. 2024 20:17 |
URI: | https://espace.inrs.ca/id/eprint/15039 |
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