Lack of Th17 Cell Generation in Patients with Severe Burn Injuries1
Immunodeficient patients with severe burn injuries are extremely susceptible to infection with Candida albicans ( C. albicans ). In addition to Th1 cells, IL-17-producing CD4 + T cells (Th17 cells) have recently been described as an important effector cell in host anti- Candida resistance. In this s...
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Veröffentlicht in: | The Journal of immunology (1950) 2011-08, Vol.187 (5), p.2155-2161 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Immunodeficient patients with severe burn injuries are extremely susceptible to infection with
Candida albicans
(
C. albicans
). In addition to Th1 cells, IL-17-producing CD4
+
T cells (Th17 cells) have recently been described as an important effector cell in host anti-
Candida
resistance. In this study, therefore, we tried to induce Th17 cells in cultures of severely burned patient PBMC by stimulation with the
C. albicans
antigen (CAg). In the results, the biomarkers for Th17 cells (IL-17 production and intracellular expression of IL-17 and RORγt) were not displayed by burn patient PBMC stimulated with CAg, while these biomarkers of Th17 cells were detected in cultures of healthy donor PBMC stimulated with CAg. Burn patient sera were shown to be inhibitory on CAg-stimulated Th17 cell generation in healthy donor PBMC cultures; however, Th17 cells were induced by CAg in healthy donor PBMC cultures supplemented with burn patient sera that were previously treated with anti-IL-10 mAb. Also, the biomarkers of Th17 cells were not induced by CAg in healthy donor PBMC cultures supplemented with rIL-10. IL-10 was detected in serum specimens derived from severely burned patients. These results indicate that Th17 cells are not generated in burn patient PBMC cultures supplemented with CAg. IL-10, produced in response to burn injuries, is shown to be inhibitory on Th17 cell generation. The high-susceptibility of severely burned patients to
C. albicans
infection might be influenced if burn-associated IL-10 production is intervened. |
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ISSN: | 0022-1767 1550-6606 |
DOI: | 10.4049/jimmunol.1003235 |