T(reg) cells may regulate interlukin-17 production by modulating TH1 responses in 1,3-ß-glucan-induced lung inflammation in mice.
J Immunotoxicol
; 10(3): 253-61, 2013.
Article
en En
| MEDLINE
| ID: mdl-22963429
ABSTRACT
1,3-ß-glucan is considered a fungal biomarker and exposure to this agent can induce lung inflammation. Complement activation plays an important role in early immune responses to ß-glucan. Previous studies showed that T-regulatory cells (Tregs) regulated 1,3-ß-glucan-induced lung inflammation by modulating the maintenance of immune homeostasis in the lung. Both interleukin (IL)-17 and TH17 cells play pivotal roles in inflammation associated with lung disease and share reciprocal developmental pathways with Tregs. However, the effect of Tregs on IL-17 and TH17 responses in 1,3-ß-glucan-induced lung inflammation remains unclear. In this study, mice were exposed to 1,3-ß-glucan by intratracheal instillation. To investigate the effects of Tregs on IL-17 and TH17 cells in the induced lung inflammation, a Treg-depleted mice model was generated by administration of anti-CD25 mAb. The results indicated that Treg-depleted mice showed more severe pathological inflammatory changes in lung tissues. Tregs depletion reduced IL-17 expression in these tissues, and increased those of TH1 cytokines. The expression of IL-17 increased at the early phase of the inflammation response. There were no significant effects of the Tregs on expression of RORγt and IL-6 or the amount of CD4(+)IL-17(+) cells in the lungs. When taken together, the late phase of the 1,3-ß-glucan-induced inflammatory response in the mice was primarily mediated by TH1 cytokines rather than IL-17. In contrast, the early phase of the inflammatory response might be mediated in part by IL-17 along with activated complement. Tregs might be required for IL-17 expression during the late phase inflammatory response in mice. The increased IL-17 mRNA observed during the 1,3-ß-glucan induced inflammatory response were attributed to cells other than TH17 cells.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Neumonía
/
Zimosan
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Regulación de la Expresión Génica
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Linfocitos T Reguladores
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Células TH1
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Interleucina-17
Límite:
Animals
Idioma:
En
Revista:
J Immunotoxicol
Asunto de la revista:
ALERGIA E IMUNOLOGIA
/
TOXICOLOGIA
Año:
2013
Tipo del documento:
Article